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_uccessor tl) the renowned Manual Medicine: Diagnostics and Manual Medicine: ·Inerapy.
this richly illustrated. logically organized book. while clinically oriented. presents both the
theory and practice of the expanding field of musculoskeletal medicine. Its aim is to fully
integrate and coordinate the relatively young firld of manual medicine with classic medical
school teaching, based on currenL biomechanical and evidence-based knowledge. Without
pleJudice the book includes the posillve aspects of osteopathic and chiropractic examination
and treatment tpchnique within the context of a functionally meaningful musculoskeletal
managpment approach.

Whllt> the particular examination and related treatment techniques are described in detail.
tile layour facl1itate both a quick overview and sufficient detaJi, when needed. The accom­
panying text describes and correlates possible pathologic findings. Other chapters cover the
history of manual medi ine, examination and Lreatment principles. and the application of
biomechanics and muscle physiology La the variolls non-surgical hands-on approaches,
including myofascial trigger point treatmtnt. Emphasis is given to anatomical descriptions
of muscles Jnd their palpatory assessment as well as techniques to treat shortened muscles.
The concept of muscle imbalance is presented.

Relationships between pain and specific variables are juxtaposed Jnd graphically represented.
Rarionaltreatmenl approaches are deScribed. ranging from "wait-and-see" recommendations
to further medical work-up and indications for surgery. SpecifiC musculoskeletal disorders Jre
reViewed in detail.

Highlights:
• Systematic presentation, from three-dimensional anatomy to function and pain
• Over 1000 illustrations. dispenslllg with [he need for lengthy text passages
• LogICal presentation of speCific disorders
• "Action" photographs for examination and treatment
• Full-color drawings and photographs with superimposed graphics clearly depicting
lhe joints and areas of each body region
• Physiological explanations and further requirements substanliclting the use of
m;mipulative medicine
• Well arranged examination techlllques for the entire person

Muscu/oskeleral Manual Medicine will be indispensable to professionals who treat the person
with acute and chronic musculoskeletal problems, providing access to the broadest possible
cumamentarium based on today's knowledge and insights.

The Americas Rest of World

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Library of Congress Cataloging-in-Publication Data is available Important note: Medicine is an ever-Changing science undergoing
from the publisher. continual development. Research and clinical experience are contin­
ually expanding our knowledge. in particular our knowledge of
proper treatment and drug therapy. Insofar as this book mentions
any dosage or application. readers may rest assured that the authors.
editors. and publishers have made every effort to ensure that such
references are in accordance with the state of knowledge at the time
of production of the book.
Nevertheless. this does not involve. imply. or express any guaran­
Parts of this book are an authorized and revised translation of the 5th
tee or responsibility on the part of the publishers in respect to any
German edition of Manuelle Medizin: Diagnostik and the 3rd German
dosage instructions and forms of applications stated in the book.
edition of Manuelle Medizin: Therapie. published and copyrighted
Every user is requested to examine carefully the manufacturers'
1997 by Georg Thieme Verlag. Stuttgart. Germany. This book also
leaflets accompanying each drug and to check. if necessary in con­
includes revised and updated material taken from the 1 st edition of
sultation with a physician or specialist. whether the dosage schedules
Manual Medicine: Therapy and the 2nd edition of Manual Medicine:
mentioned therein or the contraindications stated by the manufac­
Diagnostics. published and copyrighted 1988 and 1990. respectively.
turers differ from the statements made in the present book Such
by Georg Thieme Verlag. Stuttgart. Germany.
examination is particularly important with drugs that are either rarely
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IV

Copyrighted Material
List of Contributors

Hubert Baumgartner, MD Carl Granger, MD


Former Chief of Rheumatology Professor of Rehabilitation Medicine
Schulthess Clinic University at Buffalo
Zurich, Switzerland School of Medicine and Biomedical Sciences
Executive Director
Daniel Buehler Uniform Data System for Medical Rehabilitation
Physiotherapist Amherst
Fluntern High School Sports Center New York, USA
Department of Physiotherapy
Zurich, Switzerland Dieter Grob, MD
Professor
Douglas Chang MD, PhD
, Head of Spine Surgery
Assistant Professor Schulthess Clinic
Chief, Physical Medicine and Rehabilitation Zurich, Switzerland
Department of Orthopedic Surgery
University of California, San Diego Norbert Gschwend, MD
San Diego, CA, USA Professor and Former Chief Surgeon and Chairman
Schulthess Clinic
Jill Chomiak, MD, PhD Zurich, Switzerland
Associate Professor
Head of Pediatric Orthopedic Department Jochen F. Loehr, MD, FRCSC
University Hospital IPVZ and 1 st Medical Professor of Orthopedics
Faculty of Charles University ENDO-Clinic
Hospital Na Bulovce Hamburg, Germany
Prague, Czech Republic
Chetan Malik, MBBS
Beat Dejung, MD, PhD Clinical Instructor
Physical Medicine Specialist Rehabilitation Medicine
Rehabilitation and Rheumatic Diseases Department of Physical Medicine and Rehabilitation
FMH Swiss Medical Association University at Buffalo
Winterthur, Switzerland School of Medicine and Biomedical Sciences
Uniform Data System for Medical Rehabilitation
Tomas Drobny, MD Amherst
Orthopedic Surgeon, Lower Extremity New York, USA
Schulthess Clinic
Zurich, Switzerland Anne Frances Mannion, MD, PhD
Head of Department
Toni Graf-Baumann, MD, PhD Research and Development
Professor Schulthess Clinic
Managing and Scientific Director Zurich, Switzerland
German Society of Musculoskeletal Medicine
Managing Director Urs Munzinger, MD
German Society for the Study of Pain Orthopedic Surgeon FMH
German Pain Society Head of Orthopedic Surgery. Lower Extremities
Teningen. Germany SChulthess Clinic
Zurich, Switzerland

v
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Manohar M. Panjabi, PhD Wolfgang Trautmann
Professor Emeritus Physiotherapist
Former Director Biomechanics Research Director of Physiotherapy
Yale University School of Medicine Sports Medical Center Bern
New Haven, Connecticut, USA Permanence Clinic Bern-Hirslanden
Bern, Switzerland
Bogdan P. Radanov, MD
Professor Beat Waelchli, MD, DC
Head of Pain Center PRISMA Spine Surgery Zollil<erberg
Schulthess Clinic Center for Chiropractic Zurich
Zurich, Switzerland Zollikerberg, Switzerland

Pascal Rippstein, MD Barbara Weber Schneider, MD


Chairman of Foot and Ankle Department Dietlikon, Switzerland
Schulthess Clinic
Zurich, Switzerland Richard D. Weissmann, PT, OMT I
Physiotherapy Practice and Clinic
Beat R. Simmen, MD, PhD Head of Faculty
Chairman Upper Extremity and Hand Surgery David G. Simons Academy
Schulthess Clinic Winterthur, Switzerland
Zurich, Switzerland

Acknowledgements

As editors of a textbook with a history of 25 years and a In this respect we thank Thieme Publishers for assigning
track record of five editions in German and two editions in two such skillful collaborators to assist in the project from
English, Japanese, Spanish, and Italian respectively, we beginning to end.
have been supported, in particular, by Mr. Brian Scanlan, We would like to thank the Schulthess Clinic Zurich for
President of Thieme Publishers. The idea and concept for offering its infrastructure. In particular, Mr. Andreas
the current, completely reworked book Musculoskeletal Li.itscher, head of the documentation center of the Schult­
Manual Medicine was strongly supported by the Executive hess Clinic, who supported us since 1986 and who contrib­
Director, Dr. Clifford Bergman, who saw the advantage of uted in a major way in the production process while chang­
the new concept. ing from the classical style to complete digital desktop
Fusing the previous two books, introducing several new publishing. Those who went through the process greatly
chapters, and enhancing the layout and presentation of the appreciate such professional help. A special thanks also
material was quite an undertaking. We would therefore goes to the research assistants from the Schulthess Hospi­
like to extend our special thanks to Mrs, Annie Hollins, tal, Mr. Dave O'Riordan and Mr. Charles McCammon, who
Editorial Assistant, and Ms Elisabeth l(urz, Production Edi­ helped us with the references and coordinated contacts
tor, from Thieme Publishers, who did more in the course of with all of the collaborators.
the translation and production of the book than anyone We, as editors, experienced that a project of this nature
would expect from a publishing house. Both ladies now is not just an individual effort. It requires a tremendous
understand the concept of musculoskeletal manual medi­ amount of teamwork to produce a textbook such as this.
cine as they not only contributed to the production of the
book but also used their intellectual capacity to identify
and eliminate mistakes that occurred in the fusion process. The Editors

VI

Copyrighted Material
Preface on the Occasion of the 25th Anniversary

The current textbook Musculoskeletal Manual Medicine has, two authors influenced immensely how we would learn to
in terms of medical publishing, a long and interesting his­ think about and approach new research projects that
tory. Although this book has a new format, completely would investigate principles of mechanisms and how they
reworked and reorganized, the original ideas presented relate to clinical signs and symptoms. This resulted in a
25 years ago still hold true. To the surprise of many-both wonderful friendship and thoughtful scientific collabora­
within and outside the field-probably no other back pain tion, and nearly 50 papers in peer-reviewed journals.
treatment interventions have been studied as exhaustively Knowing the quality ofThieme Publishers, we presented
in biomechanical studies and randomized clinical trials as them with our hand-made book for consideration. In 1983,
manual medicine procedures. Thieme Publishers courageously published a book which at
During the past 25 years, interest in the field has steadily that time appeared to be quite an exotic project: the first
increased, both on the part of the public and patients, and German edition of Manual Medicine: Diagnostics. We think
on the part of orthodox medicine. Manual medicine has that this important decision served everyone well.
gone from having an "outsider" role to being a logical part Soon after the first edition, and being educated within
of the armamentarium of today's musculoskeletal physi­ the framework of the rather young Swiss Medical Associa­
cian. Again, history is a good teacher. tion for Manual Medicine, we visited well-established edu­
In the mid 1970s, cr, M RI, SPEcr, and PET scans capable cational institutions of osteopathic medicine in the USA
of investigating structures and tissues potentially respon­ that already held university status, as well as those colleges
sible for primary symptoms such as pain and altered struc­ of chiropractic accredited by the Swiss health system to
ture and function were not available to patients presenting educate Swiss chiropractors. The close exposure and col­
with musculoskeletal disorders. However, with the increas­ laboration with experts of osteopathic manual medicine
ing interest in and fascination of applications of technology such as Philip Greenman, Myron Beal, and Bob Ward, and
in patient care, the physician's hands as a diagnostic and from the chiropractic profession, Scott Haldeman, not only
therapeutic tool were commonly neglected, particularly in offered us new dimensions and aspects of manual medicine
the assessment of such musculoskeletal disorders as so­ but also taught us to respect and collaborate equally with
called nonspecific or mechanical low back and neck pain. doctors of osteopathic medicine and doctors of chiroprac­
In the late 1970s our attention was attracted by a small tic.
group of Swiss physicians successfully using manual med­ Wolfgang Gilliar, DO, currently Professor at the New
icine approaches, both diagnostically and therapeutically. York College of Osteopathic Medicine of the New York
We became students of the prominent Swiss rheumatolo­ Institute of Technology, translated the book, and it was
gist, Dr. Max Sutter, who taught us one-on-one how to use presented to the English-speaking market in 1984.
our hands to palpate the changes of different tissues in the Following the experience gained from our exposure to
human body such as the skin, subcutaneous tissues, osteopathy and chiropractic on the occasion of the 7th
muscles, and tendons. The principle idea was to try to International Congress of the FIMM (International Federa­
identify the anatomical structures and relationships re­ tion of Manual Medicine) in Zurich in 1983, we invited the
sponsible for pain and altered function in a joint or spinal leaders in their particular field to what is now known as the
region. Fischingen Conference. There, within 1 week, the common
The first two authors, together with the orthopedic denominators of manual medicine, osteopathy, and chiro­
surgeon Dr. Tomas Drobny, set down their experiences of practic were openly and collegially discussed. We realized
the nearly 3-year educational process in the first German that many of the diagnostic and therapeutic approaches
edition of Manual Medicine: Diagnostics (Manuelle Medizin: appear similar or deviate only slightly from each other-as
Diagnostik), with a print run of a total of 10 copies of a book far as the biomechanical model is concerned-and their
based on our own hand colored drawings, the starting point approach and applications may have been shaped, at least
of a long medical journey. Many of the original drawings in part, by their professional context and philosophy.
from this very first edition in 1980 are still used in the In the 1980s relationships between exponents of manual
current textbook, now redrawn and following a layout medicine and classical orthodox medicine were somewhat
that was created, yes, with sophisticated publishing tech­ tense. In other words, traditional universities. at least in
nology. At that time we were already impressed by the Europe, seemed rather reluctant to integrate the diagnostic
seminal research papers and textbook on clinical bio­ and therapeutic aspects of manual medicine within the
mechanics by Augustus White and Manohar Panjabi. These framework of what could be best medical practice. Around

VII
Copyrighted Material
Preface

the globe, the trend of and call for evidence-based ap­ in Switzerland, which offers postgraduate teaching to doc­
proaches became more important, not only in academic tors and physiotherapists in the field of musculoskeletal
practice but in medical practice altogether. In this regard, manual medicine.
we received quite a strong message from one of the most The current English edition, Musculoskeletal Manual
prominent and respected pioneers in spine research, Pro­ Medicine, has been completely reworked and integrates
fessor Alf Nachemson from Giitheborg, Sweden. After send­ the newest aspects of clinical biomechanics. clinical prac­
ing him the first edition of the English bool< for review, his tice. and evidence-based approaches to diagnose and treat
answer was swift and to the point: "I will not read your musculoskeletal disorders conservatively. including the
bool< unless it has been scientifically proven." Our first preventive programs.
reaction was quite human, but giving Dr. Nachmeson's For this new book. we invited Wolfgang Gilliar. O.
comments a second thought, we were markedly influenced meanwhile close friend and exponent of osteopathic med­
by them, as was our further development. The first author icine and well-known not only in the USA but also in
returned from clinical practice and started his residency in Europe. to be coauthor. Having translated our initial texts
neurology to obtain education and particularly scientific (Manual Medicine: Diagnostics and Manual Medicine: The/'­
tools to investigate and fulfil Nachemson's request. In this apy). being a physiatrist. and ever interested in furthering a
respect, the close collaboration with Manohar Panjabi and meaningful understanding of principles and mechanisms.
his research team, as well as the opportunity to perform he developed his own personal approach and expertise
cadaveric experiments in the highly sophisticated labora­ from the start. His contribution to the new English edition
tory of the Moris MUlier Institute in Bern was a lucky has been major and the editors are very thankful that
coincidence to the advantage of the development of Mus­ Wolfgang accepted the invitation to help shape and signifi­
culoskeletal Manual Medicine, which further contributed to can tly contribute to the current book.
our personal improvement of understanding and clinical As editors and authors. we are highly satisfied with the
skills. We realized, thanks to Nachemson's hard lesson, that several editions in different languages, with the first and
clinical experience-while serving as a good starting current edition spanning 25 years. The new edition. which
point-is not enough, and actually carries a risk of being now has become an entirely new book. reflects our per­
led in the wrong direction. sonal development as physicians. and at the same time is
The scientific approach, which we as authors of the witness to the growing acceptance of this form of medicine
current book implemented in the framework of our think­ within the medical community. We realize this brings with
ing, dominated our next steps with the intention to search it the responsibilities we editors need to take into account
for evidence of those phenomena which we felt by using when presenting new teaching material.
our hands for diagnosis and treatment. The exposure as Truly this book has become a "trans" book: transconti­
active members of the leading spine societies such as the nental and transdisciplinary. integrating neurology UO).
International Society for the Study of the Lumbar Spine, the internal medicine (VO). physical medicine and rehabilita­
Cervical Spine Research Society, and the Spine Society of tion (WG). rheumatology (WS). sports medicine (HS). and
Europe, also influenced our development and, being con­ physiotherapy (TI). With the invaluable input from all the
fronted with spine surgery in particular, we learnt the contributors. it is our sincere wish that the reader is stimu­
limits of conservative approach including those of manual lated to move beyond professional boundaries and look at
medicine. We respected the limits and, while understand­ the "soul" of the topic at hand.
ing the great advantages of modern spine surgery, we dis­ This may be a topic-hopefully with more research re-
cussed and recommended surgical procedures to our pa­ suits. ideally with its own new ideas and forms of inves­
tients when necessary to reduce pain and improve func­ tigation- in a book in another 25 years from now.
tion.
In 1997 we completely reworked and restructured the
books and invited three new editors to enhance and im- Jiff Dvorak
prove the fifth German Edition with their experience and Vac/av Dvorak
expertise. Wolfgang Ci/liar
In this form the book became a major educational tool Werner Schneider
within the Swiss Medical Association of Manual Medicine, Hans Spring
one of the most successful and active medical associations Thomas Tritschler

VIII

Copyrighted Material
Contents

1 Manual Medicine-An Overview .......


Somatic Dysfunction and Tender Points .... ...... 126
The Spondylogenic Reflex Syndrome .......... ,. 127

Historical Perspective ..................... .

Recent International Perspective ...............

Effectiveness, Outcomes, and Open Questions ..... , 2 7 The Structural and Functional

Neuro-Musculoskeletal Examination ... 135

2 Definitions and Principles of Manual


Introduction .. .. ... ... ..... ... ......... 135
Medicine Diagnosis and Treatment..... 4
Observation ("LOOK") . ... .. ... ... ... ...... 137
Palpation ("FEEL").... ... ..... ... ..... .... 137

Definitions and General Principles ............ , . 4

Motion Testing ("MOVE") .......... ..... .... 140

Treatment Principles of Various Manual Medicine


Functional Examination of the Muscles
Techniques.......................... . 16

and Myofascial Structures ... . . ... ... .. .... 142

Provocative Tests .... ... ........ ..... .... 144

3 Biomechanlcal Principles of the Spine Rational Selection of the Appropriate Laboratory


and JOints ......................... 41
and Adjunctive Diagnostic Studies. .. ......... 144

General Biomechanical Principles...............


41
Clinical Biomechanics of the Spine............. .
41 8 Rational Selection of Appropriate
Biomechanics of the Upper Cervical Spinal joints
Low-Risk Treatment Interventions..... 145
(CO-C1-C2) .......................... 44

Introduction .......... ..... ... ......... 145

Biomechanics of the Lower Cervical Spine (C3-C7).... 54

Examination Levels in Relation to the Diagnosis


Vertebral Artery ........................ . 61

and Treatment of Musculoskeletal Disorders. ..... 148

Biomechanics of the Thoracic Spine .............


64
Correlation of the Various Clinical Parameters .. .... 149

Biomechanics of the Thorax and Ribs ............ 65

Biomechanics of the Lumbar Spine ............ . 66

Biomechanics of the Pelvic Girdle ..............


69 9 Indications and Contraindications for
JOint Motion and Biomechanical Correlations 78 Conditions with Potentially Increased
Risk of Treatment . ................. 160

4 Neurophysiology of the Joints


Diagnosis: Lumbar Disk Herniation .... ... . . .... 160
and Muscles ...................... . 81
Diagnosis: Lumbar Spinal Stenosis
(Central and/or Foraminal Stenosis) . . . • ... .... 161
Neuropathophysiology of the Apophyseal joints ..... 81

Diagnosis: Cervical Disk Herniation . ... ..... .... 161

Articular Neurology ....................... 81

Diagnosis: Cervical Spinal Stenosis... ... ........ 162

Functional Pathology of Muscle............... .


87
Diagnosis: Acute Soft-Tissue Injury to the Cervical Spine 162

What's on the Horizon - When Manual Medicine


Diagnosis: Chronic Phase of Soft-Tissue Injury
and Molecular Medicine Meet .............. . 98

to the Cervical Spine . .... ... ... ..... .... 163

Diagnosis: Cervicogenic Vertigo


5 The Pharmacologic and Psychologic (Including Cervical Migraine) ... ... ...... ... 163

Treatment of Chronic Pain ........... .


99 Diagnosis: Spondylolisthesis with Spondylolysis
B. D. Radanov in the Lumbar Spine. ........ ... .. ... .... 164

Understanding Pain Mechanisms. ... ..... .... .. 99 Diagnosis: Bony Malformations of the Vertebral Column,
Pharmacologic Treatment of Chronic Pain ...... ... 102
Malformations of the Spinal Cord. ... .. ... . . .. 164
Psychologic Aspects of Pain Treatment ......... "
110 Diagnosis: Osteoporosis (in the Presence of Pathologic
Vertebral Fractures) . ..... ... .... ........ 164

Diagnosis: Ankylosing Spondylitis (Bechterew Disease):

6 Nonradicular Pain: Spondylogenic


Acute Inflammatory Changes ... ... ..... .... 165

and Myofascial Pain Syndromes . .. . ... 113

Diagnosis: Ankylosing Spondylitis (Bechterew Disease)

Referred Pain............. ... ........ ... 114


without Clinical Signs of Acute Inflammation " ... 165

Myofascial Pain Syndromes .... ... ........ ... 118

The Postural Pseudoradicular Syndrome .... ... ... 122

IX
Copyrighted Material
Contents

Diagnosis: Inflammation of the Vertebral Column Neurologic Disorders Associated with Back Pain. . .... 222
in Association with Chronic Rheumatoid Arthritis.... 166 Cervicogenic Vertigo and Headache ............. 226
Diagnosis: Abnormal Segmental or Regional Spinal Degenerative Disorders of the Spine. . . . . . . • ..... 231
Hypermobility (Congenital or Acquired) ......... 166 Metabolic and Rheumatologic Disorders
Diagnosis: Patient on Anticoagulation Medication..... 166 Affecting the Spine...................... 232
Organ-related Pain and Pseudo Spine Pain ......... 238
Orthopedic Spinal Disorders.................. 240
10 Evidence Base in Manual Medicine for
Spondylosis, Spondylolysis, Spondylolisthesis,
the Treatment of Back Pain Syndromes:
and Spinal Stenosis........ .............. 241
Background, Status, and Practice ..... 167
Spinal Deformities........................ 243
A. F. Mannion, j. Dvorak, W. Gilliar
Clinical Disorders and Syndromes of the Upper Limb. 252
Brief Historical Background. .................. 167
B. R. Simmen, W. Gilliar
Effectiveness and Cost Considerations: Evidence
General Comments ..... . ... . ............. 252
and Recommendations.................... 167
The Shoulder. .......................... 252
Requirements for Successful Manual Medicine
Common Shoulder Disorders ................. 252
Management: The Individual Practitioner......... 170
The Elbow. ............................ 268
Surgical Interventions: A Brief Overview . .......... 268
11 Informed Consent, Complication Elbow Disorders ......................... 270
Assessment, Quality Control, The Wrist.......................... , .. 276
and Documentation ................ 171 Wrist Disorders.......................... 276
T. Graf-Baumann, W. Gilliar Clinical Disorders and Syndromes of the Lower Limb. 287
Informed Consent within Patient Care.......... .. 171 The Hip .............................. 287

Complication Assessment ................... 171 j. F. Loehr, W. Gilliar

Quality Control in Manual Medicine; Disorders of the Hip....................... 287

Continuing Education..................... 172 Hip Disorders in Childhood ..... . . • . . . . . . . • .. 289

Documentation Requirements................. 173 Hip Disorders in Adults..................... 296


The Knee ............................. 301
T. Drobny, U. Munzinger, W. Gilliar
12 Patient Outcome and Follow-Along Patients Younger than 45 Years........... . . • .. 302
Measures. ........................ 174
Patients Older than 45 Years ............. . , .. 307
C Granger, C Malik
Disorders of the I<nee....... . ........... . .. 309
Introduction............................ 174 The Foot and Anlde. ...................... 317
s
The LlFEware M System .. . .. .. . .. ........ 174 . . •
P. Rippstein, W. Gilliar
LlFEware System Measures ................... 175 Disorders of the Toes ....... . ... . . ......... 317
LlFEware System Domains ................... 175 Heel Pain ............................. 324
Case Study............................. 184 Foot Deformities. . . . . . . . . • . . . . . . . . • ...... 328
Conclusion............................. 185

15 Structural and Functional Diagnosis


13 Imaging Studies of the Spine . ........ 186 and Treatment of the Spine, Ribs.
Pelvis. and Sacroiliac Joint. .......... 331
Introductory Remarks . . . • • . . . . . . . . • • ....... 186
Cervical Spine........................... 187 Structural Examination and Functional Treatment
Thoracic Spine . ......................... 201 of the Cervical Spine .................. 331
Lumbar Spine and Pelvis .................... 203 Palpation of Bony Landmarks:
Bulging Lumbar Disks and Disk Herniations.... . .... 212 Cervical Spine ......................... 331
Nuclear Medicine Studies......... . .......... 213 Irritation Zones (IZ) Associated with the Cervical Spine . 332
Structural Examination of the Cervical Spine........ 335
CO through C7 ....... .. .............. 335
14 Selected Clinical Syndromes. ......... 214
Evaluation: Active Motion Testing of Flexion, Extension,
Clinical Disorders and Syndromes of the Spine. .... 214 Rotation, and Side-Bending. ................ 335
D. Grob, j. Dvorak, W. Gilliar CO through C7 ....................... 337
Pain and the Spine: A Brief Overview of Approach 214 Evaluation: Passive Motion Testing of Flexion, Extension,
Nerve Roots and Nerve Root Pain........... 216 Rotation, and Side-Bending . ................. 337

Copyrighted Material
Contents

C3 through C7 ............... . 339 C1-C2 ..................... . 360


Evaluation: Rotation in Extension ..... . 339 Self-Mobilization: Rotation Restriction .... 360
CO through C7 ............... . 340 C1-C2 ..................... . 361
Evaluation: Provocation Position and Motion Testing NMT 2: Rotation Restriction (Neutral Position) . 361
of the Vertebral Artery by Rotation and Reclination. 340 C1-C2 ........ ... ............ 363
CO through C3 ..... ........... . .. 341 NMT 3: Rotation Restriction (Neutral Position) . 363
Evaluation: Active Motion Testing for Inclination C1-C2 .. .. . .. ..... ......... ... 365
and Reclination.. ............ . ...... 341 NMT 2: Rotation Restriction (with Upper Cervical Spine
CO through C3 ... ... ..... ... .. ... . 342 Fully Flexed) ......................... , 365
Evaluation: Passive Motion Testing for Inclination C1-C2 ............................. 366
and Reclination, ........ ... ... ...... 342 NMT 3: Rotation Restriction (with Upper Cervical Spine
CO-C1............ .. ... ........ .... 343 Fully Flexed) . .......... .. ...... 366
Evaluatian: Passive Motion Testing of Axial Rotatian C2-C3 . ............. ., ...... 367
and Evaluation ofJoint Play ......... 343 NMT 2: Rotation Restriction .. 367
CO through C3 ... .......... 344 C2-C3 ..... ......... 368
Evaluation: Side-Bending at the CO-C1 NMT 3: Rotation Restriction ... .. 368
and c/-o Segments ......... . 344 CO through C3 . . ... . . ... ... 369
C1-C2.................. . 345 Mobilization without Impulse: Axial Traction .... ... 369
Evaluation: Active Motion Testing of Axial Rotation... 345 CO through C3 . . ..... . .. .............. 370
C1-C2............................ " 346 Mobilization with and without Impulse: Cervical Traction 370
Evaluation: Passive Motion Testing of Axial Rotation . 346 CO through C3 .. ... .. ... ....... 371
C1-C2....... ..................... 347 Mobilization with Impulse (Thrust): Traction . ... ... 371
Evaluation: Passive Motion Testing of Axial Rotation CO through C3 ....... ... ... ... ..... ... 372
at c/-o and Evaluation ofJoint Play ... ... .. 347 Mobilization with Impulse (Thrust): Axial (Longitudinal)
C1-C2.... .. .............. ..... 348 Traction..................... . 372
Evaluation: Forced Rotation of the Axis with CO through C2 ................. 373
Side-Bending, Axis Rotation ......... . 348 Mobilization with Impulse (T hrust): Traction 373
C2-C3................... 349 C1 through C3 ................ . 374
Evaluation: Passive Rotation Testing.... . 349 Mobilization with Impulse (Thrust): Rotation Restriction. 374
CO through C3 ....................... 350 CO through C3 ..................... 375
Evaluation: Translatory Gliding at CO through 0 . . .. 350 NMT 2 and NMT 3: Inclination (Flexion) Restriction . 375
C4 through C7 ... . .. ... ..... .. ... .. .. 351 C2 through C7 . . ..... . ............. . 376
Evaluation: Passive Flexion, Extension, Side-Bending, Mobilization without Impulse: Rotation Restriction. . 376
and Rotation Motion ..................... 351 C2 through C7 .. ... .. ... ... ... . . ... ... 377
C3 through C7 ...... .. ... ........ ..... 353 Mobilization with Impulse (Thrust): Rotation Restriction. 377
Evaluation: Passive Flexion, Extension, Side-Bending, C1 through C6 .. ........ ... ... ..... ... 378
and Rotation Motion .. . ...... ..... . . .. 353 Mobilization with Impulse (Thrust): Rotation Restriction. 378
C3 through C6 .............. ........ 354 C2 through C6 .. ..... ... ... ........... 379
Evaluation: Translatory Gliding... ..... ...... 354 Mobilization with Impulse (T hrust): Rotation Restriction. 379
Functional Treatment of the Cervical Spine. ...... 355 C2 through C7 .. ... .. ... . ....... ... ... 380
CO-C1.... ............. .. ........... 355 Mobilization with Impulse (T hrust): Rotation Restriction. 380
Mobilization without Impulse: Inclination (Flexion) C2 through C7 ........... 381
and/or Reclination (Extension) Restriction . ........ 355 NMT /: Rotation Restriction ...... . 381
C1-C2. ........................... 356 C2 through C7 ... . .......... 382
Mobilization without Impulse: Rotation Restriction .. .. 356 Self Mobilization: Rotation Restriction 382
CO-C1.... ..... ..... ... ..... ... 357 C2 through C6 ............. 383
NMTI: Inclination (Flexion) and/or Reclination NMT 2: Rotation Restriction ... . 383
(Extension) Restriction..................... 357 C2 through C6 .......... . 384
CO-C1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358 NMT 3: Rotation Restriction .... 384
Self-Mobilization: Inclination (Flexion) and/or Reclination C2 through C6 ........... 385
(Extension) Restriction........ ........ 358 NMT 2: Side-Bending Restriction 385
C1-C2........ . ............ . ....... 359 C2 through C6 ........... . 386
NMTI: Rotation Restriction .................. 359 NMT 3: Side-Bending Restriction ......... . 386

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C7 throughT 5.................... 387 13 throughT10........................ 411


Mobilization with Impulse: Extension Restriction. 387 Mobilization with Impulse (Thrust): Rotation Restriction. 411
C7 through T6............. 388 T4 through T9......................... 412
Mobilization with Impulse: Traction ........ 388 Mobilization with Impulse (Thrust): Rotation Restriction. 412
C6 through T4.................... 389 T5 through T12........................ 413
Mobilization with Impulse (Thrust): Rotation Restriction 389 Mobilization with Impulse (Thrust): Rotation Restriction. 413
C5 through T4.................. 390 T6 through T12........................ 414
Mobilization with Impulse (Thrust): Mobilization with and without Impulse (Thrust):
Rotation and Side-Bending Restriction..... 390 Rotation Restriction ...... 414
C6 through 13.................. 391 Rib I ...................... 415
Mobilization with Impulse (Thrust): Rotation Restriction 391 Mobilization without Impulse:
C6 through T5 ........................ 392 Exhalation (Inferior) Restriction (Supine) . 415
NMT 1 and Self-Mobilization: Extension Restriction ... 392 Rib I .................... . .. 416
Structural Examination and Functional Treatment Mobilization without Impulse:
of the Thoracic Spine and the Ribs ........ 393 Exhalation (Inferior) Restriction (Seated) . 416
Palpation of Bony Landmarks .............. 393 Rib I ...................... 417
Irritation Zones Associated with the Thoracic Spine. 394 Mobilization with Impulse (Thrust):
Irritation Zones Associated with the Ribs ....... 395 Inferior-Anterior Rib Motion Restriction........... 417
Structural Examination of the Thoracic Spine and Ribs. 398 Ribs VI through XI ...................... 418
T1 through T12 ................. 398 Mobilization without Impulse:
Evaluation: Passive Motion Testing of Flexion Anterior and Lateral Rib Motion Restriction 418
and Extension................. . 398 Ribs IV through XII .................... 419
T1 through T12 ................
399 Mobilization without Impulse and NMT 1:
Evaluation: Motion Testing of Side-Bending Anterior and Lateral Rib Motion Restriction ....... 419
(Coupling Patterns)............. 399 Ribs IV through XII ..................... 420
T1 through T12 ............. . 400 Mobilization without Impulse and NMT 1:
Evaluation: Motion Testing of Rotation 400 Anterior Motion Restriction....... 420
Thoracic Spine (T1 401 Ribs III through VIII........... 421
Evaluation: Springing Test........ 401 Mobilization with Impulse (Thrust):
T1 through T8 .............. 402 Anterior Motion Restriction.................. 421
Evaluation: Passive Thoracic Mobility with Active Ribs VI through XII ...................... 422
Assistance (Testing for Resiliency) . 402 Mobilization with Impulse (Thrust):
Rib I . . . . . . . . . . . . . . . . . . . . . . . . . 403 Anterior and Lateral Motion Restriction.......... 422
Evaluation: Active and Passive Motion Testing . 403 Ribs IV through X.......... . . . . . . . . . • .. 423
Ribs III through XII ................ 404 Mobilization with Impulse (Thrust):
Evaluation: Testing of Active Rib Motion during Anterior-Inferior Motion Restriction............ 423
Inhalation and Exhalation............. 404 Ribs IV through XII .. ................... 424
Ribs VI through XII ................ 405 NMT 2: Anterior Motion Restriction ............ 424
Evaluation: Individual Rib Motion Testing during Structural Examination and Functional Treatment of
Respiratory Effort................... . 405 the Thoracolumbar Junction and the Lumbar Spine 425
Functional Treatment of theT horacic Spine and Ribs... 406 Palpatory Identification of the Bony Landmarks in
T6 through T12 ........................ 406 the Lumbar Spine..................... 425
Mobilization without Impulse: Rotation Restriction 406 Irritation Zones Associated with the Lumbar Spine.... 425
13 through T1 0 ................ 407 Structural Examination of the Lumbar Spine........ 428
Mobilization without Impulse and NMT 2: L1 through L5 ............... . ......... 428
Extension Restriction.............. 407 Evaluation: Static Examination of Posture of the Lumbar
T6 through T12 ............... 408 Spine and Pelvis with Patient Standing and Sitting .... 428
Mobilization without Impulse and NMT 2: L1 through L5 ....................... 429
Rotation Restriction ............. 408 Evaluation: Active Motion Testing of Lumbar Flexion,
13 through T1 0 ........................ 409 Extension and Side-Bending with Patient Standing 429
Mobilization with Impulse (Thrust): Flexion Restriction .. 409 L1 through L5 .................. 430
T4 throughT10 ........................ 410 Evaluation: Passive Motion Testing of Flexion
Mobilization with Impulse (Thrust): Rotation Restriction . 410 and Extension .................. 430

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II through l5 ...................... 431
Evaluation: Position of Pubic Bones......... . 456

Evaluation: Passive Motion Testing of Side-Bending Sacroiliac joint ................... .


457
(Lateral Bending).................... 431
Evaluation: Provocation Testing by Pressure
II through l5 ..................... 432
on the Zone of Irritation and Nutation Motion
Evaluation: Passive Motion Testing of Rotation, at the Sacroiliac joint............
457
Side-Bending, Flexion, and Extension ....... . 432 Sacroiliac joint, Iliolumbar ligament ..
458
II through l5 ..................... 433
Iliolumbar ligament ...... 460
Evaluation: Passive Motion Testing of Rotation . 433 Evaluation: Functionol Testing........
460
lumbar Spine (ll through l5) . ... .... .. .. ... 434 l2-Sacrum .. ... ......... . .. .
461
Evaluation: Springing Test ............... . 434
Evaluation: Provocative Testing of the Iliolumbar
Functional Treatment of the lower Thoracic Ligament by Pressure and Induced Movement 461
and lumbar Spine ..............
435 Sacroiliac joint, Sacrospinous ligament ..... 462
T10 through l5 ..................
435 Evaluation: Functional Testing........... .
463
Mobilization without Impulse and NMT2: Sacroiliac joint, Posterior Sacroiliac ligament.. 464
Rotation Restriction in the Thoraco-Lumbar junction Evaluation: Functional Testing......... . 465
and the Lumbar Spine............ . 435 Sacroiliac joint, Sacrotuberous ligament . 466
T12 through l5-S1 .............. 436 Functional Treatment of the Sacroiliac joint
Mobilization without Impulse and Traction: and the Pelvic Girdle ..... 467
Flexion Restriction .. . . .. . .. . ...
. . 436 Sacroiliac joint ........ . 467
T12 through l5-S1 .............. 437 Mobilization without Impulse:
Mobilization without Impulse and NMT 2: Posterior Motion Restriction ......... . 467

Rotation Restriction .............. 437 Mobilization without Impulse and NMT 1:


II through l5-S1 ............... 438 Anterior Motion Restriction ......... . 468

Mobilization with Impulse (Thrust): Rotation Restriction. 438 Mobilization without Impulse:

II through l5 ......................... 440 Anterior Nutation Restriction of the Sacrum NMT 1:

Mobilization with Impulse (T hrust): Rotation Restriction. 440 Posterior Rotation Restriction of the Ilium... 469

II through l5 . ................... ..... 442 Mobilization without Impulse:

Mobilization with Impulse (Thrust): Anterior Nutation Restriction of the Sacrum/

Rotation and Flexion Restriction ... ......... ... 442 Posterior Rotation Restriction of the Ilium .... 470

l2 through l5 ........................ , 444 Mobilization with Impulse (Thrust) Variation 1:


Mobilization with Impulse (Thrust): Rotation Restriction. 444 Anterior Motion Restriction ............ . 471

T10 through l5 ........................ 445 Mobilization with Impulse (Thrust) Variation 2:


NMT 1 and Self-Mobilization: Rotation Restriction 445 Anterior Motion Restriction ..... . 473
II through l5-S 1 ..... 446 Mobilization with Impulse (Thrust):
NMT 2: Flexion Restriction .... 446 Flexion Motion Restriction ...... . 475
II through l5-S1 ................ . 447 Mobilization with Impulse (Thrust):
NMT 3: Flexion Restriction .......... . 447 Anterior and Inferior Motion Restriction 477
Structural Examination of the Pelvis and Mobilization with Impulse (Thrust):
Sacroiliac Joint.................. . 448 Anterior and Inferior Motion Restriction 478
Palpatory Identification of the Bony landmarks Sacroiliac joint and ilium. .. ... ....... 479
of the Pelvic Girdle and the Sacroiliac joint . 448 NMT 1: Ilium Extension Restriction. ....... ..... 479
Irritation Zones Associated with the Sacrum,
the Sacroiliac joint, and the Pelvis ....... 448
16 Structural Diagnosis and Functional
Structural Examination of the Sacroiliac joint
Treatment of the Limbs. . ...... 480
and the Pelvic Girdle ................ 451
Pelvic Girdle. Sacroiliac joint .. ..... .... 451 Shoulder joint and Elbow, Hand, and Fingers. 481

Evaluation: Passive Motion Testing Uoint Play). 451 Evaluation: Functional Screening Examination to Give

Evaluation: Leg Length Difference ........ 452 a Rough Evaluation of Normality or Pathology in the

Evaluation: Patrick or "FABER-Test" ....... . 453 Upper Limb Within 1 Minute .............. . 481

Evaluation: Spine Test, Active Motion Testing Structural Examination and Functional Treatment

for Nutation Movement............ . 454 of the Shoulder ..............


482

Evaluation: Standing Flexion Test, Nutation Structural Examination of the Shoulder .......... 482

in the Sacroiliac joint . .................... 455

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Shoulder joint ............... . 482 Structural Examination and Functional Treatment

Evaluation: Shoulder Surface Anatomy of the Elbow ......................... 510

and Bony Landmarks .............. 482 Structural Examination of t he Elbow. . ....... .... 510

Evaluation: Active Motion Testing with Emphasis Evaluation: Elbow Inspection.. ............... 510
on Muscle Strength Assessment . . .. .. ... .. 484 Evaluation: Active Elbow Flexion and Extension . .... 511

Evaluation: Passive Internal and External Rotation. 485 Evaluation: Passive Elbow Flexion and Extension...... 512
Evaluation: Passive Internal and External Rotation Evaluation: Varus and Valgus Stress to Elbow joint .. .. 513
of Glenohumeral joint Codman Test.. . .. .... ... 486 Evaluation: Active and Passive Pronation and Supination 514

Evaluation: Painful Arc for Impingement Active Motion Evaluation: Passive Pronation and Supination,
Testing. Painful Arc (0-120°) . .... ............ 487 End-Feel and Palpation of the Proximal Radioulnar
Evaluation: Active Motion Testing and Upper Painful Arc and Humeroradial joint. .. .. ... . .. . ........ 515
120°-150° (180°) ....................... 488 Evaluation: Axial Traction. . ..... .... . .... ... 516
Evaluation: Global Shoulder Strength Test Evaluation: Translation of Proximal Radioulnar jOint . 517

for Rotator Cuff................ 489 Evaluation: Isometric Contraction of Wrist Extensors


Evaluation: Active Abduction, Rotator Cuff Strength Test, against Resistance ........... 518

including Supraspinatus Muscle jobe Test......... 490 Evaluation: Palpation of Ulnar Nerve 519
Evaluation: Active External Rotation, Strength Testing Functional Treatment of the Elbow.. 520
of the Rotator Cuff, Testing of Infraspinatus Mobilization without Impulse: Traction . . . • 520

Muscle Strength......................... 491 Proximal Rad ioulnar joint.......... . 522

Evaluation: Active Motion/Strength Testing of Internal Mobilization without Impulse: Anterior and Posterior. 522

Rotation, Rotator Cuff Strength Test, Subscapularis Structural Examination and Functional Treatment

Strength Test ........................ 492 of the Wrist and Hand ................ 523

Evaluation: Resisted Flexion and Supination at the Elbow Structural Examination of the Wrist and Hand.. .. ... 523
while Palpating the Biceps Tendon..... 493 Evaluation: General Screen ........... . . . • . .. 523
Evaluation: Instability Apprehension Test Evaluation: Wrist and Hand General Screening
(Passive External Rotation Test)..... 494 Movements .......................... 524

Evaluation: Glenohumeral Instability Evaluation: Wrist and Hand Tests for Active Mobility/
(Anteroposterior Direction) . .. ..... .. .... ... 495 Neurological Integrity .................. 525

Evaluation: Glenohumeral Anterior Instability Testing .. 496 Evaluation: Median Nerve Function to Thumb
Evaluation: Laterol Traction.... .. .. . ...... .. . 497 (Bottle Sign)........................ 526
Evaluation: Translation in Inferior Direction Evaluation: Test of Ulnar Nerve, Abduction
(Glenohumeral joint)............... 498 and Adduction of Fifth Finger . ... ....... 527

Evaluation: Translation in Anterior Direction Evaluation: Test of Ulnar Nerve Function (Froment Sign). 528
(Glenohumeral joint)............... 499 Evaluation: Ulnar and Median Nerve Compression Tests
Evaluation: Translation in Posterior Direction Using Two-point Discrimination and the Phalen Test. 529

(Glenohumeral joint)............. 500 Evaluation: Passive Wrist Extension; Extensor Tendon


Evaluation: Posterior Translation of the Palpation .......................... 530
Sternoclavicular joint.............. 501 Evaluation: Passive Flexion and Palpation
Evaluation: Inferior-Anterior Translation of the Carpal Bones ....... ..... . . ... 531

of the Sternoclavicular joint................ 502 Evaluation: Wrist and Hand Palpation of Flexor Tendons. 532
Evaluation: Translation of the Acramioclavicular joint. 503 Evaluation: Passive Flexion and Extension . ........ 533
Functional Treatment of the Shoulder. 504 Evaluation: Passive Ulnar and Radial Deviation .. .... 534
Shoulder joint ................... . 504 Evaluation: Passive Motion at Metacarpophalangeal
Mobilization without Impulse: Traction ..... . 504 and Interphalangeal joints .. .......... . . .... 535
Mobilization without Impulse: Inferior Direction . 505 Evaluation: Screening of Finger Power... 536
Mobilization without Impulse: Posterior Direction . 506 Evaluation: Selective Extension of Fingers
Mobilization without Impulse: Anterior Direction . 507 with Adjacent Fingers Fully Flexed .......... 537

Sternoclavicular jOint ........ . 508 Evaluation: Dorsopalmar Translation of the Distal


Mobilization without Impulse: Radioulnar joint ............ 538
Superior and Inferior Direction 508 Evaluation: Dorsopalmar Translation
Acromioclavicul ar joint.. 509 at the Radiocarpal joint........ 540

NMT 1: Superior Direction.... 509

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Evaluation: Darsopalmar Translation of the Scaphoid Structural Examination and Functional Treatment

and Lunate ........................ 541 of the Knee... ... . ... . . . . . .. ....... .. 569

Evaluation: Dorsopalmar Translation of the Lunate Structural Examination of the Knee. .. . .... . .. 569

and Triquetrum..................... 542 Evaluation: Inspection of the Leg Axes. Screening.


Evaluation: Translation of the Trapezium Dynamic Active Knee Movements, Especially Pivoting 569

and Trapezoid Bones, Capitate and Hamate Bone. 543 Evaluation: Knee Squatting Screening:
Evaluation: First Carpometacarpal joint Translation Walking on Toes-"Duck Walk" .......... 570

in the Radioulnar and Dorsopalmar Directions .. 544 Evaluation: Knee Translation of Patella Medially
Evaluation: Dorsopalmar Translation at the Fifth and Laterally ..................... 571

Carpometacarpal joint ................ 545 Evaluation: Inferior/Superior and Medial/Lateral


Evaluation: Translation of the Second to Fourth Translation of Patella ................ 572

Carpometacarpal joints ..... . .... ..... 546 Evaluation: Patellar Function........ 573

Evaluation: Selective Translation of All Proximal Evaluation: Active and Passive Extension...... 574

Interphalangeal joints ...... ..... ..... .. .. 547 Evaluation: Active and Passive Flexion ....... 575

Functional Treatment of the Wrist and Hand .... .. 548 Evaluation: Passive Rotation in Various Degrees
Distal Radioulnar joint . . ..... ... ....... 548 of Flexion ........................ 576

Mobilization without Impulse: Posterior-Anterior Evaluation: Traction.... . . . .. ..... .. .. 577

Direction . . . .. .......... ...... . ... 548 Evaluation: Knee Varus and Valgus Stress-Testing
Proximal and Distal Wrist joint. . .. . . . .. . . .. .. 549 of Medial and Lateral Collateral Ligaments,
Mobilization without Impulse: Traction ........... 549 and for Condition of Medial and Lateral Compartment . 578

Mobilization without Impulse: Palmar (Dorsal) Direction. 550 Evaluation: Testing for Knee Instability-Lachman Sign
Proximal Wrist joint .... ... .... . .... . .. 551 for Anterior Cruciate Ligament (ACL)

Mobilization without Impulse: Ulnar-Radial Direction .. 551 and Posterior Cruciate Ligament (PCL) . . .. .. ..... 579

Carpal BOlles.. .............. . . . .... ... 552 Evaluation: Knee Pivot Shift Test for Anterior Cruciate
Mobilization without Impulse: Dorsal-Palmar Direction 552 Insufficiency (Macintosh)..... ..... .. .. ... 580

Metacarpophalangeal and Finger joints 553 Evaluation: Testing for Anterior Cruciate Ligament,
Mobilization without Impulse: Traction ...... .. .. 553 Anterior Drawer Sign (ADS) ............. ... 581

Metacarpophalangeal and Finger joints . . . . ..... 554 Evaluation: Knee Test for Posterior Cruciate Ligament,
Mobilization without Impulse: Palmar (Dorsal) Direction. 554 Posterior Drawer Sign (PDS) ....... . . . .. . ... 582

Structural Examination and Functional Treatment Evaluation: Knee Translation Proximal T ibiofibular joint . 583

of the Hip .................... . 555 Functional Treatment of the Knee. ... 584

Screening Examination of the L ower Limb 555 Mobilization without Impulse: Traction. 584

Structural Examination of the Hip ..... 556 Mobilization without Impulse:


Evaluation: Static and Dynamic Testing; Anterior (Posterior) Direction .. 585

Trendelenburg Test, Duchenne Test .... 556 Femoropatellar Gliding ..... 586

Evaluation: Screening for Leg Length Discrepancy .. 558 Mobilization without Impulse:
Distal, Medial, or Lateral Direction . 586

Evaluation: Passive Motion Testing of Abduction Proximal Tibiofibular joint .. 587

and Adduction . ..... .... . ...... ...... .. 559 Mobilization without Impulse:
Evaluation: Passive Motion Testing of Hip Flexion . 560 Anterior-Posterior Direction .. . . . .. .... . . 587

Evaluation: Passive Motion Testing of Extension .. 561 Structural Examination and Functional Treatment

Evaluation: Passive Motion Testing of Intemal of the Ankle and Foot . ... .. ....... . 588

and External Rotation in Extension ........ 562 Structural Examination of the Ankle and Foot. . ..... 588

Evaluation: Passive Motion Testing of Internal Evaluation: Static and Dynamic Inspection ... .. . .. 588

and External Rotation in Flexion .......... 563 Evaluation: Ankle and Foot Passive Extension and Flexion. 589

Evaluation: Active Motion Testing of Abduction Evaluation: Anteroposterior Translation of Talus


and Extension ............ .. . .... . 564 on Tibia.. . . .. .. .. ..... .......... .... 590

Functional Treatment of the Hip ...... ........ 565 Evaluation: Passive Inversion and Eversion
Mobilization without Impulse: Traction (Inferior) . .. 565 (Internal and External Rotation) of Foot .. . . . . . . . 591

Mobilization without Impulse: Posterior Direction. .. .. 566 Evaluation: Dorsoplantar Translation


Mobilization without Impulse: Anterior Direction 567 of the Mid-Tarsal joints Navicular on Talus .. 592

Mobilization without Impulse: Lateral Direction ... ... 568 Evaluation: Dorsoplantar Translation Cuboid
on Calcaneus ................... 593

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Evaluation: Anteroposterior Translation of Mid-Tarsal Muscles of the Anterior and Lateral Regions of the Neck . 663
joints Cuneiform on Navicular . . ..... .. . .. ... 594 Sternocleidomastoid Muscle ................ 664
Evoluotion: Translation of Cuneiform-Metatarsal Joints. . 595 Stretching of the Sternocleidomastoid Muscle ..... 666
Evaluation: Dorsoplantar Translation of Cuboid NMT 2. . . . . . . . . . . . .. . . . . . . . ... . . . . . . 666
and Fifth Metatarsal. . . .. . .......... ... 596 Scalene Muscles. . .. ....... . .... . ....... 667
Evaluation: Test of L5 Innervation: Stretching of the Scalene Muscles............. 669
Extensor Digitorum Brevis Muscle . . 597 NMT2 . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . 669
Functional Treatment of the Ankle and Foot . . 598 Longus Colli and Longus Capitis Muscles ... . . . . . . 670
Ankle (Talocrural) joint . . . ... . . .. .. .. 598 Muscles of the Thoracic Cage and the Abdominal Wall . 672
Mobilization without Impulse: Traction . .... 598 Pectoralis Major Muscle . . ............. .... 673
Mobilization without Impulse: Stretching of the Pectoralis Major Muscle . . .... .. 675
Anterior/Posterior Restriction . . . .. ... .. . 599 NMT 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
joints at the Hindfoot (Tarsal and Tarsometatarsal Anterior Serratus Muscles. . .. .............. 676
joints) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 600 Levatores Costarum Longi et Brevis Muscles . .. ... 678
Mobilization without Impulse: Plantar/Dorsal Restriction. 600 Diaphragm. . .. ....................... 680
Toe joints . ..... .. .. .. . .. .... ......... 601 Muscles of the Abdominal Wall .............. 684
Mobilization without Impulse: Traction . .......... 601 Overview ... ... .... ....... .... .... ... 684
Mobilization without Impulse: Plantar or Stretching of the Quadratus Lumborum Muscle . .. 692 .

Dorsal Restriction. . ............. .. ... ... . 602 NMT2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 692


Muscles of the Lower and Upper Extremities. ....... 693
Iliopsoas Muscle. .......... . ........... 694
17 Functional Examination and
.

Stretching of the Iliopsoas Muscle. ........ ... 698


Treatment of Muscles. . ..... .. .. .. .. 603
.

NMT2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 698
Examination and Treatment of Muscles-Overview . . . . . 603 Rectus Femoris Muscle... ............... .. 700
Muscles of the Posterior Regions of the Neck and Back . . 606 Stretching of the Rectus Femoris Muscle . ....... 702
Trapezius Muscle . . . . . . . . . . . . . . . . . . . .. . 607.
NMT 2 . . . .. . . . ... . . . . . . . . . . . . . . . . . . . 702
Stretching of the Trapezius Muscle Hip/Thigh Adductors. .................... 704
(Descending Portion) . . . . . . . . . . . . . . . . . . . . . 610 NMT 2. . . . .. . . . . . . . . . . . . . . . . . . . . . . . . 706
NMT 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 610
.
Gluteal Muscles .. .. .. ................ .. 707
Latissimus Dorsi Muscle . . . . . . . . . . .
. . . . . . . . 611 Piriformis Muscle . . . . . . . . . . . . . . . . . . . . .. . 712
Levator Scapulae Muscle.. . . . . . . . . . . . . . . . . . 613 Stretching of the Piriformis Muscle . . . . . . . . . . . . 714
Treatment of the Levator Scapulae Muscle . . . . . . . . 615 NMT2 . . . . . . . . . ... . . .. . . . . ... . . . . .. 714
.

NMT 2 . . . . . . . . . . ..
. . . . . . . . . . . . . . . . . . 615 Tensor Fasciae Latae Muscle . . . . . . . . . . . . . . . . 715
Rhomboid Major and Minor Muscles . . . . . . . . . . . 616 Stretching of the Tensor Fasciae Latae Muscle . . ... 717
Erector Spinae Muscle Group . . . . . . . . . . . . . . . . 619 NMT2 . . . . . . . . . . . ... . . ... . . . . . . . . . .. 717
Longissimus Cervicis Muscle .. . . . . . . . . . . . . . . . . 627 Ischiocrural Muscles (Hamstring Muscles) . .. .. . . . 718
Iliocostalis Muscle . . .. .. .. . .... .. .. .. ... . 629 Stretching of the Biceps Femoris. Semitendinosus.
Treatment of Erector Spinae Muscles and Semimembranosus Muscles. . .......... .. 720
in the Lumbar Region . . . .. . .
. . . . . . . . . . . . . 633 NMT 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 720
NMT 2 . . . . . . . . . . . ... .. .
. . . . . . . . . . . . . 633 Gastrocnemius and Soleus Muscles
Splenius Muscles. . .............. . . ..... . 634 (Triceps Surae Muscle). . ... .... ........... 721
Posterior Serratus Muscles. . ................ 636 Gastrocnemius Muscle. . . ... . ...........
Suboccipital Muscles (Overview) . .. .. .. .. .. ... . 638 NMT 2 . . . . . . . . . . . . . . .. . . . .. . . . . . .... 722
Transversospinalis Muscle Group Deltoid Muscle . .. . .. ... . . .. . . . .. ... . .. 723
(Semispinalis. Multifidus, Rotatores). ..... ... .. . 644 Extensor Muscles of the Wrist .... . ...... . ... 725
Semispinalis Muscle - Overview . .. .. ... ....... 644 Wrist Extensors . .. ... .. ... . . ...... . .... 727
Semispinalis Capitis Muscle. . .. .. .. .. .. .. .... 646 NMT 2 . . . . . . . . ... . . . .. . ... . ....... . . 727
Multifidus Muscle . . . ....... .. .. .... . .. ... 648
Rotatores Breves and Longi Muscles. .... .. . .. .. . 651
18 Myofascial Trigger Point Treatment ... 728
Intertransverse Muscle Group . . . . . . . . . . . . . . . . 653
D. Buehler, B.Dejung, R. Weissmann
Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 653
Thoracic Intertransverse Muscles. . ........ .. ... 659 Rectus Capitis Major and Minor Muscles . . ....... 728

Interspinales Muscles . . . . . . . . . • . . . . . . . . . . . 662 Obliquus Capitis Inferior Muscle . . ............ 729

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Semispinalis Capitis and Cervicis Muscles . ....... 730 Psoas Muscle . . .. . . ..... .. . . .. ..... ... 747
Scalene Muscles. . .... ...... ......... ... 73' Iliacus Muscle. . . . . . . . . . . . . . . . . . . . . . • .. 748
Sternocleidomastoid Muscle . ... . ... .. ... ... 733 Gluteus Maximus Muscle. . .............. .. 749
Levator Scapulae Muscle .. .... . ..... . . . ... 734 Gluteus Medius and Minimus Muscles. . ..... ... 750
Trapezius Muscle (Upper and Lower Trapezius). .... 736 Piriformis Muscle. ... . . . . ... . . . ...... . .. 752
Serratus Anterior Muscle . ... .. ...... .. .... 738 Tensor Fasciae Latae Muscle. . . . . ... . .. . . . .. 753
Quadratus Lumborum Muscle . . . ... ......... 740
External Abdominal Oblique Muscle . . .. . .. 742
19 Home Exercise Program. . ...... .. .. 754
. . . •

Rectus Abdominis Muscle. ..... ......... ... 743


Iliocostalis and Longissimus Dorsi Thoracis! Introduction . . ..... . ..... ........ .. . ... 754
Lumborum Muscles (Erector Spinae Muscles; Exercise Section. .. . . ......... .. . . ... .... 756
the Superficial Paravertebral Muscles) .......... 744
Multifidi and Rotatores Muscles Index ..... . ... . . ........... ........ 775
(Deep Paraspinal Muscles) . .... ..... .. ..... 746

XVII
Copyrighted Material
Documentation of Examination Findings
and Treatment Techniques

Examination Findings Spine


rhe following is a scheme for documenting examination
findings, including: CO-C1,Cl-2
Direction of motion
\\ 17
Restriction of Illotion
Muscle shortening
\\\ "==:;:
. ":;= .I I' RI I"'7:':\
I In Rr

I, ,' \
" I'
Muscle weakening
Pain // H '-.
..x-tt-
.- ' /
----...;. - "-1
i , -'
" '';-
" --,. Rc
In Inclination
Rc Reclination
F Flexion
E Extension
C3-C7
I
\ \
SB Side-bending
.J/
R
r
Rotation
To the rjght
\\
, . = RI r.':\
+ Rr
I To the left '--'
4-.-4
N Nutation / , t,-:;'''T LFI LFr
f
e
El
In flexing direction
In extendinq direction
Elevation
y: ' \r-
J(
I '- :,}-"r\- r
E
IR Internal rotation
ER Externa I rotation Tl-Tl2
Ab Abduction I \ ";
' 1'1"'"
:: --:; ,
_"
__

Ad
DF
Adduction
Dorsiflexion ....:I - ,
"
- ' L;J...< ,

:-
'r
' 1'-- .' Rl r.':\
+ Rr
PF
UD
Plantar flexion
Ulnar abduction
\ I
I
r''-" '1l 1 l
.,
'" , -oy
:.LJ-M-"
J ;
/,'

RD Radial abduction 1\ It )Y'( 1\,1 LFI LFr


S Supination -''\ I r
1/' '..:..:. ' I , ,
- .... -,\
" .,J
"r" _
// I
P Pronation «I, <';
> cf:r
>rr:' ""
I
I E
L Lateral ,l' / " ) '
" -" ., 1--r
" ,:', ,,-,"\\ f
""

ll-l5

I
\ /" /I"',l I r, ' ' ' ,I \
I / /' '/.) , 'J I' "
\il,.I 1/.
/
,-
-

Ii "
,/:" r"

"","" .
.
", '
\\ "
))
RI r.':\ Rr
,I " r: /1 " \,,,(! I +
I
\,
J
i ' <'�'L)
( l..<y;' LFI LFr
/ ·l· l y(F) ,
>tu- )
"
\'
E
1,-
I ''''I
" w ,
r ,-I 1'\

SACRUM
I '-S'"
Nt Nt
/: \\\e6L c
,
/ �.
\
I
. J =- 'l\
,I '
-"..... \ ' . ' - " ' I.f"-
-I,

n-\ \'/'_ \/! ,/ (' \


Il. )1
-\': 'I.L '_' . ' . \ Ne Ne

XVIII

Copyrighted Material
Upper Extremity lower Extremity

EL

Ad
I {' --!
-f!!-
E
ER
Ab
Ad

IR
~ E

\...:.;/
Ab

ER

\ \
F F
\

E E

p 5 Ad
F Ab
RD UD

'-Y
5 p

/'7:\+ F

Symbols for Documentation of Motion Restriction, Muscle Weakness, Pain location

I Normal range of motion Shortened muscle

t Slightly restricted Weakened muscle

t Very res tricted Localized pain

t Almost completely restricted (and ankylosis) Referred pain

t Pain at end of motion 0 Irritation zone/trigger point

XIX
Copyrighted Material
Symbols for Documentation Symbols for Documentation
of Examination Findings of Treatment Techniques

Mobilization without impulse = MWOUT


FixationjSta bilization
"'V7 • Mobilization direction

~
Mobilization with impulse = MWITH
Palpation
• Mobilization direction

NMTl

/:;:::=::J Active flexion


• Mobilization direction

NMT2

§ Active extension •


Mobilization direction
Stretch direction

NMT3
Active rotation
• Mobilization direction

/:;:::=::J Passive flexion


NMT2 and NMT3
• Isometric contraction

Passive extension Trigger point treatment

-.-.----------.------

Passive rotation I Fixation - by therapist

Fixation - by patient

xx

Copyrighted Material
1 Manual Medicine-An Overview

Historical Perspective understanding of the three-dimensional anatomy, biome­


chanics, neurophysiology, and pathophysiology of the lo­
Manual medicine, one of the oldest healing arts, constitutes comotor system. ClinicaJJy, the practitioner is caJJed upon
that medical discipline in which practitioners apply their to make as accurate a structural and functional diagnosis as
hands skiJJfuJJy in both the diagnostic and therapeutic possible before instituting the appropriate treatment tech­
management of painful neuro-musculo-skeletal disorders nique for the individual patient.
and various diseases. Over time, the field of manual med­
icine has developed and refined its own approaches and
strategies through specific, and at times unique, examina- Recent International Perspective
tion and treatment techniques. More recently, various
components of the manual medicine armamentarium During the past 50 years, and in particular since the 1970s,
have been adopted by and integrated into general medical manual medicine has experienced unprecedented growth
practice, as weJJ as specialties such as Neurology, Orthope­ and acceptance not only by the general population but also
dics, Physical Medicine, Rehabilitation, Rheumatology, and by some of the traditionally orthodox branches of medi­
Sports Medicine. At present, primarily four professional cine. This increase may in part be attributed to the strong
groups routinely rely on using this form of medicine in interest by a small group of pioneering allopathic physi­
patient management, albeit to varying degrees: the aJJo­ cians in Europe, who expanded upon the initial teachings
pathic and osteopathic physicians, chiropractors, and phys­ by John Menell Sr., M.D. (Mennell, 1951) and some of the
ical therapists (Dvorak et ai., 2001). techniques brought to Europe by a nucleus of osteopathic
Despite the high number of manipulative procedures physicians and chiropractors trained in the United States.
performed every year, the number of major complications The German term "Manuelle Medizin," or manual medi­
is rather low. However, when significant complications do cine, which describes a series of treatment applications
occur, they can assume disastrous outcomes. In particular, using one's hands, is now the standard term used for
the classic "thrust techniques," more recently defined as manipulative medicine in most of Europe. The "modern"
the mobilization-with-impulse techniques and in the ver­ era can be traced back to the Swiss physician Nageli
nacular referred to as the "pop-and-crack maneuvers," (1843-1922), who described a series of "Handgriffe"
carry an inherently greater risk of potentiaJJy severe com­ (hand applications) for cervical manipulations in 1894
plications than the low-velocity, low-amplitude soft-tissue (Harris and McPartland, 1996). This was approximately 20
approaches. Thus, the techniques that are regarded as par­ years after the introduction of osteopathy by Andrew Tay­
ticularly risky require the practitioner considering their use lor Still, M.D. in the United States. Sollmann ( 1981) believes
to pay special attention to the indications and contraindi­ that Nageli had been introduced to osteopathic treatment
cations, within the context of the entire clinical picture. It techniques through some of his Swiss patients who had
seems reasonable to suggest that the high-risk thrusting gone to the United States for treatment.
techniques be performed exclusively by those professio­ Professor Robert Maigne of Paris, France, studied under
nals who have received adequate formal training and who Stoddard and Beal at the London College of Osteopathy, and
have developed the particular skills necessary to perform introduced his exaggeration technique (Maigne, 1964). An­
them correctly. other French physician, Arlen, introduced what he refers to
In contrast, the non-thrust techniques, recently termed as atlas therapy, a technique in which the patient remains
the mobilization-without-impulse techniques and gener­ in the sitting position (Arlen, 1990).
ally referred to as the soft-tissue techniques, represent In the United J(ingdom, the physician Cyriax (1904­
techniques that have been associated with less risk than 1985) (Cyriax, 1984) is arguably the most prominent British
the impulse techniques. The non-thrust techniques have figure in Manual Medicine and Rehabilitation (Harris,
found useful application in a number of fields that empha­ 1993). John MenneJJ Sr., M.D. introduced and emphasized
size the functional components of the neuro-musculo­ the importance of joint play in the examination and treat­
skeletal system. In particular, this is seen in Physical Med­ ment of the synovial joints (MenneJJ, 1951).
icine and Rehabilitation, and its associated physical and Prague in the Czech Republic became a center for stud­
occupational therapeutic management approaches. For ies in manipulation under such prominent physicians as
any of the manual medicine treatment approaches to be Henner, Jirout, Lewit, and Janda (Harris, 1993; Lewit, 1999).
successful, it wiJJ be indispensable to obtain a precise The professional exchanges between Lewit and a number

1
Copyrighted Material
Manual Medicine-An Overview

of osteopathic physicians from the United States led to a communication between a small group of medical doctors
cross-dissemination of knowledge and an amalgamation of in Europe and their osteopathic colleagues in the United
various techniques. This was particularly the case with the States (who in the U.S.A. have the same privileges and
non-thrusting techniques based on muscle energy origi­ practice rights as their allopathic colleagues) are some of
nally described by Ruddy and Kettler, and later presented the tangible factors that have contributed to the continued
by Mitchell and Greenman (Greenman, 1996; Mitchell and international exchange of ideas in both the basic sciences
Mitchell, 1995, 2001). Janda contributed to the field of and clinical practice.
myofascial pain syndromes by introducing specific muscle Both the medical (MD's and US-educated DO's) and the
rehabilitative techniques and proprioceptive retraining nonmedical approaches of manual medicine (chiropractic,
that intend to correct clinical muscle imbalance syndromes physical therapy, and other forms) have become an integral
Uanda, 1978). part of today's complementary as well as mainstream med­
Evjenth and Hamberg of Sweden (Evjenth and Hamberg, icine. Probably indicative of developments around the
1985) expanded on Janda's post facilitation stretch tech­ globe, a recent Australian study of 2000 general practi­
niques of proprioceptive neuromuscular facilitation by in­ tioners supports the generally accepted notion that physi­
cluding the antagonist-relax techniques (Harris and cians are open to further training in complementary and
McPartland, 1996). manual therapies (Cohen et aI., 2005). As with any other
Thus, the international growth of manual medicine did form of medicine, there continues to exist the need for
not take place in a vacuum. While the modern era of further scientifically based education and research.
manual medicine can trace its history to the seminal im­
pulses in osteopathy and chiropractic-building on and
expanding upon the traditions of the bone setters-the Effectiveness, Outcomes,
growth and development in recent years is the result of and Open Questions
collaborative efforts among the various international
groups and different schools of thought. Chapter 10 of this book takes a closer look at the current
In 1958, representatives from the various international evidence-based considerations applicable to manual med­
medical groups convened at the first international meeting icine. Here, we present a brief overview of manual medi­
in Switzerland. This led to the establishment of the Interna­ cine and its use in the area of back pain.
tional Federation of Manual Medicine (FIMM) at a later To date there exists no double-blind study that has
meeting in London, with society meetings occurring on a unequivocally "proved" the efficacy of manipulative treat­
triennial basis ever since. In September 1983, a group of 34 ment. Some studies, however, appear to support the notion
manual medicine practitioners from 12 countries, repre­ that by using a rational management approach that in­
senting eight schools, and conversing in seven languages, cludes a manual medicine component the duration of an
convened at a seminar following the Seventh International initial painful episode or a recurrent exacerbation may be
Congress of the FIMM in Zurich, Switzerland. Known today shortened, which in turn can significantly diminish work
as the "Fischingen Conference," this meeting of the world's absenteeism. In Switzerland, back pain alone causes the
experts began the movement toward standardization of loss of 1.5 million workdays. Back pain or degenerative
language in the field, and the establishment of study and changes affecting the spine are the second most frequent
clinical trials in the future (Dvorak et aI., 1984). During the cause of partial or full disability in Switzerland. In Germany,
1998 FIMM Congress meeting in Australia, the American 80% of the population is reported to suffer from back pain,
Osteopathic Association joined the FIMM. Associations in and a third of the population between the ages of 35 and 50
South Korea and Canada joined in 2003. Today, the FIMM years is reportedly affected by chronic lower back pain. A
has a membership basis that spans nearly 30 national third of all absenteeism is due to symptoms related to the
societies. In the mid-1990s, the founders of the San Fran­ musculoskeletal system. Back pain is one of the most fre­
cisco International Manual Society, Ores. Friedman, Gilliar quent reasons for early retirement.
and Glassman helped develop the standards for a medical During the past 20 to 30 years, the field of manual
osteopathic post graduate teaching program for physicians medicine has begun to critically analyze its own successes
in the DGOM (Deutsche Gesellschaft fUr Osteopathische and failures. Efforts have been made to scientifically sup­
Medizin). Prior contacts through Ores. Philip Greenman, port or refute patients' or practitioners' claims of successful
Ed Stiles, Myron Beal, Robert Ward from Michigan State treatment results obtained with manipulative treatment.
University College of Osteopathic Medicine facilitated the The elimination and replacement of antiquated and non­
international communication. specific terms such as "subluxation," "osteopathic lesion,"
In summary, the increased interest of and acceptance and "joint blockage" with scientifically acceptable terms
by the public on one side and the growing international was a step forward in facilitating communication not only

2
Copyrighted Material
Effectiveness. Outcomes. and Open Questions

around the world but also between the basic scientist and tolerated exercises and activities? Then, would activity
the clinician. alone- that is, any type of physical activity-suffice over
For instance. it remains an open question whether spe­ time to minimize recurrences and maintain the patient's
cific techniques such as the rotatory manipulative thrust­ pain-free episodes?
ing maneuvers are-as surmised by some-able to "displace The rehabilitation approaches for the musculoskeletal
the nucleus pulposus" and "unload" the facet joints or system have been expanded by the addition of specific.
decompress the affected nerve roots. It remains a matter individualized training therapy programs that address the
of conjecture whether and to what extent the intradiskal patient's overall level of functioning, well-being, and fit­
pressure is actually increased as a result of manipulative ness. In addition to addressing the patient's restricted
treatment. It is also not clear whether certain manipulative range of motion, reduced strength, and cardiovascular
procedures are able to free up a wedged meniscoid in the and muscular endurance, a detailed coordination and pro­
cervical spine. Another hypothesis postulates that manip­ prioceptive training program has become an integral part
ulative intervention results in considerable stimulation of of today's rational approach to a comprehensive rehabil­
the mechanoreceptors. with subsequent presynaptic inhib­ itative effort.
ition of the nociceptive afferent impulses at the level of the Possible adverse side-effects and the potential for sig­
spinal cord dorsal horn. Experimental studies are under nificant complications have led the field of manual medi­
way to explain the effect of manual medicine intervention cine to modify the classic (primarily "thrust") techniques.
by invoking the effects of enkephalins. The good contact between the European schools and the
As increasing numbers of manipulations are performed osteopathic physicians in the United States has encouraged
annually. it would appear that patients' symptoms might the learning of mobilization-without-impulse techniques
be improved acutely with manipulative procedures. De­ and their integration into the treatment armamentarium of
spite the growing interest and various studies so far. it is manual medicine physicians in Europe. The non-thrusting
still not clear whether manipulative maneuvers are able to techniques aim to introduce stretch to the noncontractile
reduce the overall number. frequency, duration, and inten­ soft-tissue structures such as ligaments and the jOint
sity of painful recurrences. capsules. It is postulated, albeit not conclusively proven,
In clinical practice, the following two key questions are that these mobilization techniques may displace the nu­
awaiting more definitive answers: cleus pulposus as well. More recently, there has been a
trend toward viewing the locomotor system as the
1. What is the most appropriate frequency with which a neuro-musculo-skeletal system, a concept that is reflected
particular joint or body region can be or should be in the field of manual medicine. The neuromuscular ther­
subjected to manipulative maneuvers? apy (NMT) approach, for instance, utilizes the reflexogenic
2. Is it possible to prevent or reduce painful episodic re­ mechanisms during the post isometric relaxation of the
currences by specific manipulative procedures? And if agonistiC muscles and the reciprocal inhibition of the an­
so, what is (are) the most appropriate type(s) of treat­ tagonistic muscles. Such progressive practice has secured a
ment approaches, treatment frequency, duration, and permanent place within modern manual medicine. Not
intensity? surprisingly, the active integration of the patient in his or
her treatment is of significant benefit.
It is hoped that future state-of-the-art research will provide According to Isaacs and Bookhout (2002), perhaps the
satisfactory answers to the above and many other ques­ greatest contribution from manipulative medicine is the
tions. For instance, the need to help a patient achieve evolution o f a diagnostic framework defining the various
muscular balance between the tonic postural and the pha­ dysfunctions that affect the musculoskeletal system, with
sic muscles is a concept that seems to have been embraced the goal of restoring function. This requires a thorough
clinically. While the assumption might be correct that study and understanding of and competence in three­
future painful musculoskeletal recurrences can be reduced dimensional functional anatomy, biomechanics, and neuro­
through such a muscular rehabilitation routine, specific physiology. This is expected to help the treating physician
studies are needed to help us determine the most suitable view and treat the patient within the context of compre­
program of stretching, strengthening, and muscular aero­ hensive bio-psycho-social medical care, with an emphasis
bic conditioning. Or would it be sufficient to treat the on the aspects of both structure and function within the
patient with the appropriate manual techniques, which is neuro-musculo-skeletal system.
simply followed by appropriately dosed and patient-

J
Copyrighted Material
2 Definitions and Principles of Manual Medicine Diagnosis

and Treatment

has commonly been used in the literature to reflect the


Definitions and Ceneral Principles
"high-velocity, low-amplitude" type of maneuvers applied
to the spine.
Manipulation and Mobilization Treatment
Techniques
Mobilization
Following the Fischingen Conference in Switzerland "Mobilization" is described in the United States as a soft­
(Dvorak et aI., 1984) the following clinical definitions tissue and articulatory type of treatment, and includes
have been utilized in the international community during other techniques such as myofascial release and muscle
the past 20 years (Dvorak et aI., 2004). In general, a dis­ energy. In Europe, this term refers to articular mobilization
tinction is made between manipulation and mobilization in the absence of thrusting forces.
techniques. Manipulative techniques typically employ a
thrusting type of maneuver, known as the classical "manip­ Thrust or Impulse Techniques
ulation"; techniques that do not use this maneuver are Both of these terms describe the same entity, with "thrust"
categorized as mobilization techniques. being preferred in the English language, and "impulse"
being more common in the European schools.
Manipulation In this text, the terms mobilization-witl1-impulse and
In the United States, manipulation refers to any therapeutic mobilization-witl1out-impulse are employed, and the indi­
procedure in which the hands are used to treat the patient. vidual treatment techniques are described as manipulative
It is therefore a rather general term in this usage. or mobilizing procedures, respectively (Dvorak et aI., 1984)
In Europe, manipulation refers to what is described in (Table 2.1).
English or according to American osteopathic terminology A summary overview of some of the most commonly
as "high-velocity, low-amplitude thrust" (HVLA). used manual therapy techniques is given in Table 2.2 (after
Spinal manipulation or spinal manipulative treatment Dvorak et aI., 2004, with permission).
refers to specific manual medicine maneuvers or special
hand "applications" directed at the spine. This term that

Table 2.1 Comparison of use of the terms as mobilization and manipulation showing continental differences

Comments

Manipulation Refers usually to the thrusting A rather general term, which may When possible. and in order to
techniques. which are also known refer to any "therapeutic" proce­ avoid confusion. the newer ter­
as high-velocity/low-amplitude dure in which the hands are used minology of mobilization-with­
techniques or the mobilization­ to treat the patient or-without-impulse techniques
with-impulse techniques should be used
Chiropractic adjustment is a ge­
neric term with over 100 sub­
techniques including HVLA­
thrust and low- force techniques

Mobilization Refers essentially to any type of Usually refers to the various non­ It is best to qualify the type of
induced tissue or joint movement thrusting and soft- tissue tech­ mobilization used
which is then qualified by de­ niques
scribing the presence or absence
of impulse forces (thrust versus
non-thrust techniques, respec­
tively)

4
Copyrighted Material
Definitions and General Principles

Table 2.2 Overview of some of the most commonly used manual-therapy techniques

Mobilization with Mobilization without Soft-Tissue Techniques Commonly Used Types


Impulse Impulse

Thrust techniques Non-thrusting techniques Preparatory and/or other Swedish-type massage


Chiropractic variations individual Effleurage (stroking)
Osteopathic variations Petrissage (compression)
Friction massage
Tapotement (percussion)

Terminology note: Articulatory technique Deep pressure technique Acupressure


Thrust is also known as:
Counterstrain technique Diaphragmatic release Connective-tissue massage
High-velocity/low-am­
plitude technique Craniosacral technique Lymphatic pump technique Deep-tissue massage
Manipulation (in gener­
al) (nonspecific; limited Facilitate positional release Mesenteric release Lymphatic massage
use)
Functional technique Pectoral release Shiatsu

Muscle energy technique Stretch techniques Sports massage (variation


Lateral, linear, diagonal Swedish)

Myofascial release technique Traction Integrating/movement techniques

ligamentous sprain technique Alexander technique


Feldenkrais method
Myofascial trigger point tech­
Rolfing
nique

Neuromuscular treatment I Many other approaches that


combine many aspects of
Neuromuscular treatment II "healing"

Neuromuscular treatment III

Others (proprietary/nonpro­
prietary)

Table 2.3 Clinical motion descriptions as defined by the primary


Further Definitions and Principles of Manual axis of rotation or plane of motion
Medicine
Primary Axis Primary Plane
of Rotation of Motion
Angular Motion
rotation around Sagittal plane
The physiologic motion during both active and passive
extension the x-axis
movement in a synovial joint, e. g., the facet or apophyseal
joint or the joints of the limbs, is a combination of rolling Inclination (flex­ = rotation around Sagittal plane

and gliding motions. The architectural shape of the indi­


ion at CO to (2) the x-axis

vidual joint, along with its associated ligaments and Reclination = rotation around Sagittal plane
muscles, determines the direction and extent of this roll­ (extension at CO the x-axis

and-glide motion (Fig. 2.1). to (2)


Motion can be described by using a three-dimensional Axial rotation = rotation around Transverse
coordinate system with three primary axes, about which the y-axiS plane

rotation takes place. These axes may be designated the x-,


Side-bending = rotation around Frontal or
Y-, and z-axes. In this system, the x-axis projects laterally, the z-axis coronal plane
the y-axis projects vertically, and the z-axis projects fron­
Abduction. = rotation around Frontal or
tally. See Table 2.3
adduction the z-axis coronal plane

Elevation, = rotation around Frontal or


depression the z-axis coronal plane

5
Copyrighted Material
Definitions and PrInciples of Manual Medicine Diagnosis and Treatment

+y R ota t i on/ rolling


7
2

+z 0'. l' �i }--z +z ( '. ¥ -z

+x
+x

-y -y

v Trans la tion /
Fig.2.1 Roll and glide motions.
gliding
+y = Traction
-y = Compression
+x, -x = Lateral gliding Fig. 2.3 Joint crepitus
+z, -z = Anteroposterior gliding 1 : RolI-gliding behavior in a "smooth," unaffected "normal" joint.
A =:0 A' = Gliding 2: Roll-gliding behavior when the joint is affected by degenerative
+Y=> l = 0X = Rotation about x-axis processes.

The level of the internal coefficient of friction is directly


related to the extent of internal resistance to motion. As
long as the coefficient of friction is held at a minimum, the
internal resistance is low. Friction Can dramatically increase
as a function of progressive arthritic degenerative changes
that affect the internal structure of the joint. In the ex­
treme, this is most evident when there is bone-on-bone
contact where the coefficient of friction will have risen to a
R
level at which very little joint motion, if any, is possible
(Fig.2.2). A change in the internal coefficient of friction
from a normal, healthy state will be associated with a
discontinuous roll-and-glide pattern of motion (Fig.2.3).
Mechanically, this will negatively affect the soft tissues
associated with the affected joint, as they have to perform
"increased work," due to the uneven and discontinuous
motions to which they are subjected.
y y
Translatory Motion
Fig.2.2 Coefficient of friction. All of the synovial joints, including the apophyseal or facet
Starting position: The coefficient of friction (R) is increased when joints in the spine and the peripheral joints, allow passive
there are degenerative changes in the articular cartilage surface.
translatory motion. Translatory motion takes place in a
Phase 1: Onset of angular joint motion. Initially there is a pure
linear fashion, along the axes of rotation.
rolling motion as the friction resistance is comparatively high.
Phase 2: Continued angular motion beyond Phase 1 will be less The extent of translatory motion has a direct relation­
smooth and will often become quite jerky, while the tension in the ship with angular mobility. A decrease in angular motion is
tendons overcomes the friction resistance. always associated with diminished translatory movement
and vice verSa (Fig.2.4).
The rolling characteristics of a synovial jOint are deter­
mined by a number of variables that influence the joint's Joint Play
internal coefficient of friction. These include the joint's Joint play is the sum of all possible passive, angular, and
particular geometrical shape and articular surface and translatory motions within the neutral zone. The clinical
also the mechanical properties of the associated bone, examination of joint play requires good tactile and palpa­
cartilage, ligaments, tendons, muscles, synovial Ouid, and tory skill.
other relevant soft tissues.

Copyrighted Material
Definitions and General Principles

Reduced joint play is associated with diminished angu­


Traction/
lar motion. Joint play is usually increased in the presence of
distracion
an unstable synovial joint (facet or limb joint). However, an
increase in joint play is not always identical with an un­
stable joint and increased angular mobility. For instance,
the joint play can be increased in the presence of dimin­
ished angular mobility. Thus, it is important to remember
that an increase in joint play is independent of and not
directly related to the extent of angular motion.

Mechanical Proper ties of the Elastic Str u ctu res


Related to the Joints and Spinal Segments
Anterior translation/
gliding
Traction/distraction
The motion characteristics of the synovial joints in the
limbs and at the facets are demonstrated conceptually in Fig. 2.4 Translatory motion directions.

Figures 2.5 and 2.6 in response to different loading forces


and induced or available motion. These curves represent concepts originate from a mechanical-engineering per­
the relationship between and effects of the various me­ spective in experimental studies using cadavers. Therefore
chanical forces as a result of the interplay between factors there are several caveats.
such as a joint's architecture, ligaments, joint capsule, and First, the long-term effects of active muscular contrac­
the presence of internal joint friction, among others. These tion on joint motion have not so far been fully elucidated.

Q,I

o
LL.

Q,I
t:
o
N

....
Q,I
Z lJ
Ru ptu re/tearing Q,I
t:
o
N
Q,I Q,I
t: .
o ....
N u
U

:;:::; ....
11\ 11\
I'D Q,I
i:jj o

Distance
Physiolog ic movement Microtrauma Macrotrauma
-------;.. .

< hera e u tic r ang e


_ _ _ _p_ _ _ _ _ _ _ _ __
____ T_ _ ___ > <__ ___
r au_ma t_ ic r ang e
T_ _ _ _ _ _ _ _ _ __
_ ___>
Fig.2.S Force-distance diagram depicting joint motion for roll-glide motion and translation in the physiologic and pathologic zones as
applicable to synovial joints (peripheral joints as well as apophyseal or facet joints).

7
Copyrighted Material
Definitions and Principles of Manual Medicine Diagnosis and Treatment

Secondly, work still needs to be done on the reaction in and characteristics under different loading situations. They pri­
effects on biological materials as a result of the rate of marily affect the roll-and-glide motion in a synovial joint
loading. Such considerations, at least in theory, are thought while repositioning the joint's center through the exploi­
to explain the potential differences in effect between the tation of coupled motions (Panjabi, 1992a).
rapid high-velocity, low-amplitude impulsive techniques When subjected to mechanical stress during the various
and the more slowly performed muscle energy techniques, loading situations associated with movement, the elastic
for instance. Third, it is important to remember that the structures are able to respond in a linear fashion, but only
mechanical function of biological tissues depends on phys­ up to a certain point. Once the loading forces are removed
ical and chemical properties, which in turn are an expres­ again, the elastic structures return to their original length,
sion of their molecular composition and associated inter­ or nearly so.
actions. Lastly, it is still unclear how all of these relation­
ships change as a function of growth and maturation, organ The Plastic Zone
development, and the aging process, in addition to "nor­ If motion proceeds beyond the elastic zone, that is,beyond
mal" degenerative changes. While there is an ever-growing the elastic extreme allowed by the particular ligaments.
body of knowledge about tissue repair and healing, we are tendons, and other soft tissues, it will inevitably cause a
still unable to explain clearly why some patients respond to microtrauma in the elastic structures. Thus, in the plastic
treatment better than others. zone, the muscles, tendons, ligaments, and disks become
essentially overstretched while their macroanatomy re­
mains essentially intact.
The Load-Displacement Diagram

The shape of the load-displacement curve is primarily The Destructive Zone


determined by the following five factors: If a limb joint or spinal segment is carried or forced beyond
the respective plastic zone, then it will be subjected to
• Architectural shape of each particular synovial joint or anatomic disruption, tears, fractures. or dislocations. This
spinal segment. typically happens during injuries, where the ligaments and
• Mechanical properties of the hard (bone) and soft (car­ tendons are excessively engaged or "stressed",for instance.
tilage, ligaments, tendons, joint capsule) tissues. Thus, when entering this zone, the tendons and ligaments
• Fluid mechanical properties (synovial fluid, cartilage). are unable to withstand the stress to which they are sub­
• Joint motion characteristics (displacement type and di­ jected and will begin to show structural changes ranging
rection). from partial tears to complete rupture. In a mechanical
• Rate of the applied forces. comparison, a rope, for instance, may tear even under
relatively little stress with small loading forces if they are
The load-displacement diagram (Fig. 2.5) can be divided applied suddenly in a burst-like fashion.
into four different "zones," namely, the neutral, elastic,
plastic, and destructive zones. The width of each zone is The Zero- Force Barrier (ZFB)
subject to large variation due to the following two major The zero-force barrier marks the junction between the
variables: neutral and elastic zones. The internal forces resisting an­
gular and translatory movement account for approximately
• Architecture and shape of the individual joint or spinal 2% of those encountered at the extreme of the elastic zone
segment. as it approaches the plastic zone (Figs. 2.6, 2.7).
• Motion directions.
The PhYSiologic Barrier (PhysB)
The phYSiologic barrier of a synovial joint lies within the
The Neutral Zone elastic zone. Thus, as long as the joint is subjected to
In the neutral zone of ajoint or spinal segment, the internal motion up to but not beyond its physiologic barrier, its
resistance to angular or translatory motion is reduced to a associated structures undergo only elastic deformation,
minimum. In nonpathologic situations, it is approximately which is generally reversible. The neutral zone remains
2% of the resistance at the extreme end of the elastic zone unchanged (Figs. 2.6,2.7).
(Panjabi,1992a). The physiologic barrier represents the extreme of mo­
tion that can be reached by the patient's own active move-
The Elastic Zone ment. Further motion in the direction of the anatomic
This zone reflects the behavior of the elastic properties of barrier is still possible but requires the introduction of
tendons and ligaments as they influence a jOint's motion additional force, such as that introduced when the exam­

Copyrighted Material
Definitions and General Principles

ining physician passively guides the joint toward the ana­


tomic barrier from where the patient's active movement
came to a stop.

The Anatomic Barrier (AB)


The anatomic barrier is located in the region between the
elastic and the plastic zones. With passively induced
movement-movement introduced not by the patient but
the examiner-the anatomic barrier can be approached
without causing microtrauma. Motion induced in a limb
joint or joints of the spinal segment (e.g., facet joints) "
,

beyond the respective anatomic barrier will push the joint , )


into the plastic zone, resulting at least in microtrauma if not
macrotrauma (Figs.2.6,2.7).
Fig.2.6 Barriers of motion.
AB Anatomic barrier
The Actual Physiologic Barrier (APhB) APhB Actual physiologic barrier
The actual physiologic barrier reflects the limit of motion PB Pathologic barrier

encountered in the presence of altered, pathologic motion PhysB Physiologic barrier


R Resting position
characteristics in a joint, such as hypomobility or hyper­
ZFB Zero- force barrier
mobility. This barrier can be engaged without necessarily
involving microtrauma or macrotrauma (Figs.2.6,2.7).

The Pathologic Barrier (PB)


The pathologic barrier, also known as the restrictive barrier,
reflects the deviation from the normal limitation of motion
caused by bony and/or soft-tissue changes (Fig.2.6). In a
clinical setting, the motion is more often than not de­
creased in the form of joint hypomobility, while it can
also be increased when there is laxity of a joint, for instance
with associated hypermobility.

The Resting Position (R)


The joint's or spinal segment's resting position is main­
tained at that point or "range" where the joint play is
greatest. Pathologic structural changes and abnormal
muscle and tissue tension displace a joint's or a spinal Fig.2.7 Barriers of motion.
segment's normal resting position. The resting position AB Anatomic barrier

marks that location within the arc of normal motion where PhysB Physiologic barrier
R Resting pOSition
the joint volume is largest. Usually, in a clinical situation,
ZFB Zero- force barrier
pain intensity is registered by the patient as minimal in the
resting position, which is also known as the present neutral
position.

Joint Localization at the Motion Barrier


Treatment Plane of a Spinal Segment When the joint or spinal segment is engaged at its respec­
or limb Joint tive motion barriers (e. g., in flexion/extension, side­
bending right/left, and rotation right/left), joint play is
The plane of treatment is perpendicular to the traction reduced to a minimum, while at the same time joint stabil­
direction. Gliding or articulatory type of mobilization in a ity is greatest.
limb joint is introduced according to the convex and con­
cave rules.

9
Copyrighted Material
Definitions and Principles of Manual Medicine Diagnosis and Treatment

Convex Rule
The convex rule applies to a joint in which the distal joint
surface has a convex shape. If angular motion is restricted
due to articular degenerative changes or other structural
changes. for instance. the direction of the mobilization­
without-impulse technique is usually opposite to that of
the restricted joint mobility (Fig. 2.8).

Concave Rule
The concave rule refers to a joint in which the distal joint
surface has a concave shape. If angular mobility is restricted
due to articular degenerative changes or other structural
changes. the direction of the mobilization-without­
impulse technique is usually in the same direction as that Fig.2.8 Convex rule.

of the joint restriction (Fig. 2.9). AB Anatomic barrier


APhB Actual physiologic barrier
PB Patholog ic ba rrier
Mobility Gain
PhysB Physiologic barrier
With the pathologic barrier as a starting point for treat­ R Resting position
ment, the mobility gained as a result of treatment is de­ ZFB Zero-force barrier

fined as the amount of newly gained angular joint mobility


primarily due to increased muscle length upon the induced
muscle stretch (Fig. 2.10). When a muscle crosses two or
more joints. it may be useful to stabilize one joint while
attempting to increase the mobility in the second joint
during the stretch.

Provocation Testing
Mechanical stress directed to the various components of
the locomotor system may lead to a number of nociceptive
reactions which. ultimately, are reported by the patient as
pain. Depending on the intensity. duration. and extent of ",PhS'

and the neurophysiologic mechanisms evoked by these


pS
nociceptive reactions, the individual patient's perception
of the pain. both qualitatively and quantitatively. is subject
Fig.2.9 Concave rule.
to significant variation. Furthermore, the nociceptive reac­ AB Anatomic barrier
tions and pain alter muscle tone and/or autonomic func­ APhB Actual physiologic barrier

tions in such a way that ultimately they contribute to a self­ PB Pathologic barrier
PhysB Physiologic barrier
perpetuating vicious cycle.
R Resting position
The clinical manifestation (sign) of the nociceptive
ZFB Zero-force barrier
reactions is the irritation zone. The finding of a specific
irritation zone upon clinical examination helps to verify
objectively the presence of a segmental dysfunction. Fur­
thermore. the clinician is able to determine which motion Biomechanical Principles and Their
direction exacerbates or improves the localized irritation Clinical Correlation
zone. by introducing specific motions to the affected joint.
Thus. the behavior of the irritation zone in response to the In-vitro studies by Panjabi et al. (1994) and Grob et al.
motions induced by the examiner, and in particular that of (1993) demonstrate that joint instability is typically asso­
controlled provocative motion testing, is a helpful tool in ciated with an increased neutral zone. Both increase and
the process of rendering a differential diagnosis and choos­ decrease in angular and translatory mobility can be asso­
ing the most appropriate treatment plan. (Fig. 2.11 a. b). ciated with an increased neutral zone. An increased neutral
zone is found both with hypomobility and with hypermo­
bility. For instance. in cases where there are findings of
advanced spondyloarthrotic/degenerative changes. the

10

Copyrighted Material
Definitions and General Principles

neutral zone can be increased, even though the segmental elasticity of the associated soft-tissue joint structures, the
angular motion is diminished, e. g., the joint is found to be neutral zone is increased. In another example, flexion­
hypomobile. However, due to the loss of or reduction in extension injury to the cervical spine in patients who
have known underlying spondylotic changes can lead to
traumatic overstretching of the soft tissues, pushing the
joint(s) into the plastic zone or, worse yet, into the destruc­
tive zone. This increases the neutral zone, which can be
clinically determined by testing the affected joint(s) for
signs of instability: When the usually smooth roll-and­
glide mechanism is impaired, sudden or abrupt mechanical
stress forces will be transmitted directly to the bones,
ligaments, and tendons. Because these structures can be
viewed as "receptor organs," they play a significant role in
the coordination of motion and muscle tone. Any disrup­
tion in the interplay between smoothness of joint motion
and loading forces can lead to clinically relevant nocicep­
tive reactions and pain, which in turn can lead to changes in
the normal movement patterns, ultimately leading to clin­
Fig. 2.10 Motion gains. ically observable muscular imbalances.

I 2
Z +0Y z
Z Z
+0Y
I

l
X

Xl
+0 Y
---4-----4-- ��--l_----_+�- x
------�-----r-L- x

Fig.2.11a Provocation testing. Fig.2.11b Provocation testing.


x', y' = Pathologic motion barrier as demonstrated for rotation to x2, Z2 = The new pathologic motion barrier for passive rotation
the right of the superior vertebral partner in a spinal to the right of the superior vertebral partner in a spinal
segment segment: this correlates to the trial treatment using any
+(2lY Pathologic rotation motion to the left (e. g., left rotation of the NMT 1, 2, 3, MWITH and/or MWOUT treatment
restriction) of the superior vertebral partner in the spinal techniques
segment resulting from the muscles that are the agonists IZ Irritation zone
to left rotation Red = Shortened rotator brevis muscle on the right side
IZ = Irritation zone (muscle that is antagonistic to right rotation)
Red = The shortened rotator brevis muscle on the right (note: => Reduction of the irritation zone (IZ) by passive right
the agonist for left rotation becomes the antagonist for rotation of the superior joint partner of the incriminated
right rotation) spinal segment
- = Amplification of the irritation zone (IZ) by increasing left
rotation of the superior joint partner of the incriminated
spinal segment

11
Copyrighted Material
Definitions and Principles of Manual Medicine Diagnosis and Treatment

Application of the Biomechanical Model


to Various Therapeutic Modalities

Biomechanically. manual medicine procedures take place


in the neutral and elastic zones only. and typically do not
NMT3
enter the plastic zone (Fig. 2.12).
Depending on the individual clinical situation. the goal
NMT2
of treatment is to restore normal joint play and/or restore
as much of the normal range of motion as possible. If the
forces introduced to a joint during a manipulative maneu­ NMTl
ver are inappropriately directed or are excessive. there is
a real risk of damaging the joint and its surrounding
Mobllizatlon·wlthoul·lmpul...
tissues. especially when going beyond the joint's anatomic
barrier.
MobIlizatiQn·wtth·lmpulse/manlpulatlon
In certain clinical situations however. it may be neces­
sary to move a joint into its plastic zone. for instance in
certain manipulation procedures under anesthesia. Apart
from this exception. it should otherwise never be the goal
..
1
01
0 c: c:
of manual medicine procedures to thrust any joint into the N 0
2
plastic zone and run the risk of causing macrotrauma "! v
N
i
'5 t;
IV
'i;;
IV i
(Fig. 2.13). w l5: .!
Tissue response

Potential Risks Associated with Manual


Fig.2.12 T he different force magnitudes utilized in mobilization
Techniques: Biomechanical Considerations and manipulation techniques.

Treatment Risk as Related to the Velocity


of Mobilization Force
....
c:
As discussed earlier. there is a fundamental biomechanical ..

difference in the way a tendon is able to withstand varying .sIV


loading conditions. If the loading force is applied in quick
o
IWBI
and abrupt bursts. e. g., intermittently but with high speed. (II

then relatively little force is necessary to cause the tendon I, :I BI


to tear, either partially or completely. If the loading force is
introduced rather slowly and over a period of time. the
chance of a tendon to tear is marked Iy reduced.
Accordingly. it is reasonable to assume that the high-veloc­
ity. low-amplitude mobilization-with-impulse techniques
(MWITH) have a much greater likelihood of causing irre­
versible damage than the mobilization-without-impulse
techniques (MWOUT). Furthermore, the rapidity with
Fig.2.13 Forces used in mobilization and manipulation techniques.
which a high-velocity impulse force is introduced to ajoint
Treatment force I up to ZFB ( Zero-force barrier)
or spinal segment may be too sudden for the usual protec­
Treatment force II up to PhysB ( Physiologic barrier)
tive reflexes to respond. These two factors. the biomechan­ Treatment force III up to AB ( Anatomic barrier)
ical properties of the tissues and the elimination of the Treatment force IV beyond AB

protective reflexes. help explain how the MWITH tech­


niques can thrust the facet joint into the destructive zone
with the application of relatively little force.

72

Copyrighted Material
Definitions and General Principles

Treatment Risk as Related to the Amplitude


Microtrauma
of Mobilization Force :

I \
",

0
If manipulative treatment introduces excessive forces and ...
pushes the joint(s) beyond its/their respective anatomic ! 01
C
0
N 0
barrier(s), there is a great risk of causing tissue damage, N
'!
..
which can range from microtrauma to macrotrauma. These ."
:::I
GI .. 01
C
z tiJ 0
changes can include the following: N
01
c }
..
2
Microrrauma (Fig. 2.14) .l:!
t( 11'
i 2:
• Increase of the neutral zone.
Distance
• Reduction in the quality of the roll-and-glide motion.
Fig.2.14 Microtrauma.

Macrotrauma (Fig. 2.15)

Macrotrauma
• Increase of the neutral zone.

I \
• Adaptive, overcompensatory or even decompensatory
changes in the associated joint structures, including the
joint capsule and muscles, in an attempt control the loss
of stability.
!
2
v
i
Treatment Risk as Related to Degenerative Changes i
--------�--�
Affecting Elastic Tissue Structures Pathologic neutral zone
due to macrotrauma
Elastic tissue structures that demonstrate degenerative
Distance
changes are characterized by a reduced ability to withstand
stress, with an increased chance of structural failure. This is Fig.2.15 Macrotrauma.
represented graphically in Fig. 2.16, which depicts a con­
densed elastic and plastic zone. Thus, in treating a patient
who has known or suspected degenerative joint and/or
soft-tissue changes, the mobilization maneuvers should
be performed with as much care as possible and with as
little force as necessary. This applies to both the thrusting
(impulse) techniques and the nonthrusting techniques. GI
C
0
Treatment must always pay attention to the specific joint's GI N
01 01 GI
altered or "reset" anatomic barrier (Fig. 2.16), beyond
gN C
0
C
0
.
N N 1::
which treatment should not go. '! v :::I

l ."
..
i
.. ti01
The presence of osteophytes and spondylophytes may Z tiJ i£: Q
lead to an abrupt stop of the joint gliding motion. Inappro­
Distance
priate treatment with excessive force application may
break these structures, inevitably leading to macrotrauma.
Fig.2.16 Motion characteristics as a result of degenerative changes.
The elastic zone is decreased. Clinically, this implies the
following:

• Hard end-feel.
Degenerative Joint and Spinal Changes While the
• Loss of range of motion.
Neutral Zone is Increased
• Even small movements can bring the joint into the
destructive zone. Instability
Degenerative joint changes along with osteophyte forma­
tion reduce the rOll-and-glide as well as the gliding motion
in a joint. Not only the articular surfaces are involved; the
stabilizing structures within and surrounding the joint can
also become affected. If subject to trauma these structures

13
Copyrighted Material
Definitions and Principles of Manual Medicine Diagnosis and Treatment

Pain Reaction (Nociceptive Reaction)


.. In the presence of pain. and following the hysteresis phe­

.£ nomenon (Fig. 2.18). muscle tension may increase very rap­


id Iy. whi Ie the return is characterized by a less steep curve.

.. In the clinical situation where the pain becomes appa­


g
N
rent rather early in the arc of movement (the initial steep
..
§
N
c
o
N
portion of the curve). the associated end-feel is usually
U described as a "hard-reflexive end-fee!." On the other
:; 2
"

.. ..
t:
0::
hand. if the curve is less steep and the appearance of pain
is gradual. the end-feel is described as "soft." A soft end-feel

Distance
is usually observed. for instance. when the isotonic muscles
responsible for limiting motion have shortened (Fig. 2.18).

Fig.2.17 Instability.
Repetitive Mobilizations into the Plastic Zone and
Their Effects on Instability
QI When entering the plastic zone repeatedly. both mobiliza­
.£ tion techniques with and without impulse may cause in­
..
appropriate stretch (i. e.... overstretch ) and thus increase
the joint's neutral zone. Depending on their structural in­
..
c
0 tegrity. the soft-tissue structures may withstand the stretch
, .. .. ..
N

lJ
..
g
N
c
0
c
0 2 (reversible stretch) or may ultimately become irreversibly
N N 1::
f U U :::J stretched beyond their normal length. which would lead to
i..
U
.. segmental or joint instability.
z 0:: .!!:
Therefore one should always remember the potential

Distance risk of iatrogenic instability (Fig. 2.19).

Fig.2.18 Nociceptive reactions.


End- Feel at the Motion Barrier

QI
If the forces that are introduced with active or passive
.£ motion exceed the resistive forces at the joint's anatomic

§
N §
barrier. the joint is potentially subject to permanent dam­
N .. age.
f
!i
.. ..
..
2.. In manual medicine. the assessment of the end-feel at
z c
o the motion barrier is of great clinical significance. as it
N
U
assists in the appropriate correlation with the structural.
'i
i .!!: functional. or pain perception leve!. Through a careful ex­
amination the treating practitioner determines how much
Distance force is necessary to approach but not exceed the anatomic
barrier. The patient should be as relaxed as possible. It goes
Fig.2.19 Repetitive mobilization procedures.
without saying that the patient's entire clinical situation
should be assessed in a comprehensive and functionally
meaningful manner.
Thus. the manual medicine assessment is not done in
may be stretched beyond their normal length and ulti­ isolation but rather within the context of other relevant
mately lose their inherent elasticity (Fig. 2.17). orthopedic. neurologic. rheumatologic. physiatric. and psy-
In the presence of such tissue changes. it is thus possible chologic examinations and the necessary diagnostic stud-
that upon clinical examination there is reduced range of ies.
motion while the joint is unstable and the neutral zone is The assessment of the end-feel at the motion barrier
increased. For example. pronounced osteoarthritic changes requires great manual skills. which can only be learned in
can follow from an anterior cruciate ligament tear. accredited courses and under the supervision of clinically
experienced instructors. Only through ongoing practice

14

Copyrighted Material
Definitions and General Principles

will one be able to improve and perfect the manual and


clinical skills that are needed.
The passive motion examination of the synovial joints
(facet and/or joints of the limbs) determines the following
three major components:

• Angular range of motion.


• Joint play.
• End-feel at the motion barrier.

The manual assessment of the end-feel at the motion bar­ Fig. 2.20 Hard end-feel caused by osteophytes.
rier is of clinical significance as it differentiates between PB = Pathologic barrier
two primary possibilities:

• Hard end-feel: the resistive forces increase rapidly Shortened muscle

(steep curve).
• Soft end-feel: the resistive forces increase rather grad­
ually (shallow curve).

In addition to the joint's anatomic barriers, one differen­


tiates further between the physiologic and the pathologic
motion barriers.

Physiologic Barrier Fig.2.21 Soft end-feel.


• Shape and structural architecture of the joint; its motion PB = Pathologic barrier
limit.
• In particular the behavior of the jOint's related soft
tissues, such as tendons, ligaments, fascia, and muscles
account for this limit. Shortened Tonic Muscles
• In the unaffected joint, this represents the end of active A shortened muscle or muscle group typically causes a soft
(e. g., patient-induced) motion. end-feel as the resistive forces increase gradually rather
than abruptly, i. e., subject to plastic deformation (Fig. 2.21).
Pathologic Barrier
• Changes in/aberrations from the jOint's normal func- Hemarthrosis
tioning (in the apophyseal joint or in a limb joint). Hemarthrosis typically sets off nociceptive reactions in the
• In the affected joint, this typically represents a reduction muscles and other soft tissues associated with the affected
or loss of normal physiologic motion (hypomobility). joint. The nociceptive reactions become most apparent
• However, there may be laxity of the tissues and associ­ when the joint is carried toward the pathologic barrier
ated increased motion (hypermobility) due to structural not only due to the accompanying chemical irritation but
abnormalities (e. g., tendon rupture). also because of the increase in joint pressure secondary to
the increased intra-articular fluid. The internal joint pres-
The following four factors affect the motion barrier: (1) os- sure is least at the actual or present neutral position, and
teophytes and spondylophytes; (2) shortened tonic mus­ any change from that position usually results in an increase
cles; (3) hemarthrosis; and (4) an acute disk herniation. in pain. Thus, exceeding the critical internal joint pressure
will lead to an amplification of the patient's nociceptive
Osteophytes and Spondylophytes reactions and pain, ultimately causing a hard-reflexive end-
Osteophytes and spondylophytes change the joint's surface feel (Fig. 2.22).
structure and therefore impact on the roJl-and-glide mo­
tion of the incriminated joint. The end-feel is characteristi- Acute Disk Herniation
cally described as a hard-pathologic end-feel while the An acutely herniated disk causing sufficient mechanical
range of motion is simultaneously reduced (Fig. 2.20). compression and/or inflammatory reactions to affect the
nerve root, the perineurium. and/or the arachnoid is usu­
ally accompanied by significant pain. This precipitates a

15
Copyrighted Material
Definitions and Principles of Manual Medicine Diagnosis and Treatment

Treatment Principles of Various Manual


Noci ceptive reaction
Medicine Techniques
Inflammation

+ The following section describes the principles of major

-0 manual medicine techniques and related musculoskeletal


treatment options.

Overview
Fig.2.22 Reflex hard end-feel due to hemarthrosis.
• Mobilization-without-Impulse [MWOUT].
PB Pathologic barrier
• Mobilization-with-Impulse [MWITH].
CNS Central nervous system
MEP Muscle end plate • Neuromuscular Therapy NMT.
- Mobilization utilizing direct muscle force NMT 1.
- Mobilization utilizing the post-isometric relaxation
massive nociceptive reaction when the incriminated spinal phase NMT 2.
segment is taken to its respective barriers, and also when - Mobilization utilizing reciprocal innervation mecha­
the involved nerve and nerve roots are subjected to addi­ nisms NMT 3.
tional stretch (i. e., the sciatic nerve, femoral nerve, cervico­ • Muscle Trigger Point Therapy.
brachial plexus). - Manual techniques.
The nociceptive reactions can become so pronounced - Injection therapy.
that there is no motion possible whatsoever at the incrimi­ • Training Therapy-Reconditioning and Home Exercise
nated spinal segment. Then the pathologic motion barriers Program.
for flexion and extension are nearly identical, if not the - Stretching exercises.
same, and the end-feel is described as hard-reflexive. - Strengthening exercises.
In the Lasegue maneuver, the roots of the sciatic nerve - Self-mobilization exercises.
are subject to mechanical irritation at the level of the disk • Physical Therapeutic Modalities.
herniation when the straight leg is progressively flexed by - Cold/heat applications.
the examining physician between approximately 20' and - Electrotherapy.
70' of hip flexion. A prominent nociceptive reaction is - Ultrasound.
accompanied by sudden radiating pain and a hard reflexive
end-feel. If the end-feel elicited with the Lasegue maneuver
is rather soft, it may indicate hamstring shortening more so Mobilization- without-Impulse Techniques
than an acutely herniated disk. [MWOUT]
In the reversed Lasegue test, the nociceptive reaction is
caused by a pull at the femoral nerve. Similarly to the The following principles apply to the mobilization­
Lasegue test, the pain increases rather suddenly at one without-impulse techniques.
point in the arc of induced motion. The same maneuver is
utilized when examining for muscle length of the rectus Spine (Apophyseal or Facet Joints)
femoris muscle. Thus, a rather soft end-feel would point • Slack is taken up in the facet joints above and below the
more in the direction of a shortened rectus femoris muscle, affected vertebral segment; i. e., the spinal segments
whereas a hard-reflexive end-feel would represent a find­ above and below the restricted spinal segment are
ing commensurate with mechanical irritation of the femo­ guided to their respective barriers.
ral nerve and/or its associated nerve roots. • The operator should make every attempt to place his or
her hand over those areas that are not painful to the
patient; i. e., bony contact should be made only with
structures that lie outside of the incriminated irritation
zone.
• Mobilization proceeds in the pain-free direction.
• The direction of the mobilization forces is determined
by carefully dosed provocation or "test" maneuvers in
the assessment phase of the examination. The direction
of the applied mobilization procedure is the same as

16

Copyrighted Material
Treatment Principles of Various Manual Medicine Techniques

that in which the patients pain and nociceptive reac­


l Z
tions decrease (Fig. 2.11 a, b, Fig. 2.23). Z
+oy
• Duration of the mobilization techniques ranges between
3 and 10 seconds.
• The intensity and frequency of this technique should be
/'
carefully dosed such that the mobility in the individual
spinal segment does not exceed the joint's anatomic
barrier. ,
x
• The mobilization procedure is accomplished in a step­
+oy
wise manner by repeating the procedure three to four ----7-----��- x

times and with each step starting anew from the newly
gained barrier (Fig. 2.24).

Synovial Joints of the Extremities


• The incriminated peripheral joint (extremity joint) is
first guided to its present neutral position (resting po­
sition).
• The hands are placed as close to the joint as possible.
Usually it is the proximal joint partner that is fixated Fig. 2.23 Provocation testing.
Xl, Z 1 Pathologic motion barrier
(held stationary) while the more distal partner is being =

+0Y = Pathologic left rotation of the superior vertebra


mobilized.
IZ = Irritation zone
• The direction of the mobilization follows the convex­
concave rule.
• Traction may be introduced before the mobilization
technique itself is applied, as it may help reduce pain if it AB PhysB

is present (mobilization level l-II).


• The intensity and frequency of this technique should be
determined carefully for each particular joint while al­
ways keeping in mind not to exceed the anatomic bar­
rier (mobilization level III).

The force-time diagram (Fig. 2.25) demonstrates that while


the joint is being prepared for the mobilization technique
(positioning and set-up phase), the forces that are being
introduced to the particular joint are comparatively small.
Fig. 2.24 Stepwise motion gain upon repetitive mobilization.
As the mobilization progresses, the introduced forces in­
AB = Anatomic barrier
crease slowly until a certain point at which time they PhysB = Physiologic barrier
diminish again (duration: 3 to 10 seconds). PB = Pathologic barrier
The distance-time in diagram (Fig. 2.26) demonstrates
that the mobilization procedure starts at the joint's patho­
logic barrier. Furthermore, it shows that the gain in mob­
ility should be short of exceeding the joint's anatomic
barrier.
The mobilization-without-impulse technique is re­
peated several times, while the starting point of each step
is the newly gained barrier. With each step, the direction of
mobilization increases the joint's mobility toward the ana­
tomic barrier, thereby increasing the joint's present phys­
iologic range of motion.
When performed correctly, treatment is usually well
tolerated by the patient and should not increase the pa­
tient's initial present pain (if present).

17
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Definitions and Prindples of Manual Medidne Diagnosis and Treatment

Q)
v
...
o
.....

Mobilization

Q)
c:
Q)
OJ
2
c: Q) III
o c c: >
o
N
N 2 :e
u ::::J
.....
::::J '"
:p
VI
b
Q) '" '" :G
Z w a:: o

Position Set-up phase/"taking out the slack"

Time

Fig.2.25 Mobilization-without-impulse technique. Force-time diagram.

Q) "
v
c:

VI

C
=--
Distance gain

Mobilization

Q)
c:
o
III N
c: Q) Q) Q)
c: c: >
2 o
N S 'B
U u ::::J
:p 'P
"5
III
VI
rc
VI
rc
Z W a::

Position Set-up phase/"taking out the slack"

Time

Fig,2.26 Mobilization-without-impulse technique. Distance-time diagram,

18

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Treatment Principles of Various Manual Medicine Techniques

Mobilization- with-Impulse Technique


Joints of the limbs
(MWITH) (Classic Thrust Technique, • The affected peripheral joint (limb joint) is guided to its
"Manipulation") present neutral (resting) position.
• The operator's hands are placed as close to the joint as
The mobilization-with-impulse technique is also known as possible. Usually it is the proximal joint partner that is
the classic "thrust" technique, often referred to in the liter­ fixed (held stationary). The direction of impulse force is
ature simply as a "manipulation." perpendicular to the plane of treatment.
The following principles apply to the mobilization-with­ • The mobilization-with-impulse technique progresses
impulse technique (MWITH). from level II mobilization to level III mobilization.

Spine (Apophyseal or Facet Joints) The force-time diagram (Fig.2.28) demonstrates that dur­
• Slack is taken up in the facet joints above and below the ing the positioning of a synovial joint. the forces introduced
incriminated vertebral segment; that is, the spinal seg­ to the particular joint are relatively small.
ments adjoining the restricted spinal segment are car­ The distance-time diagram (Fig.2.29) demonstrates
ried to their respective barriers. that the mobilization-with-impulse techniques involve
• Positioning of the patient and preparation for the tech­ very brief but precise maneuvers (high-velocity, low­
nique should be performed carefully so as not to intro­ amplitude) in which the applied force moves the joint
duce or exacerbate the patient's pain. beyond its particular or actual pathologic barrier but with­
• Mobilization proceeds in the pain-free direction. out exceeding the anatomic barrier.
• The direction of the mobilization forces is determined
by carefully dosed provocation testing. The direction of
mobilization is that in which the patient-reported pain
and the nociceptive reactions decrease (Fig.2.11 a, b, Z
Zl
Fig.2.27). +0Y
• The mobilization-with-impulse technique in which the
spinous process or the articular process of the inferior

\
partner of the spinal segment is utilized will introduce
vertebral rotation in the same direction as the irritation
zone.
• Thus, the inferior vertebra undergoes rotation away
from the irritation zone. The opposite is true for the
+0Y
superior vertebral partner, which undergoes a rotation --�-------+--�---+�- X
toward the irritation zone (Fig.2.27).
--
• The force of the impulse should be carefully dosed so as
not to introduce motion beyond the anatomic barrier
(mobilization level III. Fig.2.13).
• Mobilization-with-impulse should be performed care­
fully and with great caution so as not to exacerbate the
patient's pain in the incriminated joint, or spinal region.
• When using the mobilization-with-impulse technique,
the affected segment should be treated no more than
once during the treatment session.

Fig.2.27 Mobilization-with-impulse (MWITH).


MWITH-via the superior vertebra
MWITH-via the inferior vertebra
x', Z1 = Pathologic motion barrier
+0Y = Pathologic rotation to the left of the superior
vertebral joint partner
IZ = Irritation zone

19
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Definitions and Principles of Manual Medicine Diagnosis and Treatment

QJ
U

o
L.&..

Impulse

CLo

2
! QJ QJ

I
I: I:
2 o
N
o
N

j
U u
'.;:0 '.0
Vl oil
ro "'
WJ c::

Position Set-up phase/"taking out the slack"

Time

Fig.2.28 Mobilization-with-impulse technique. Force-time diagram.

QJ
U
c:
"'
t; Distance gain
i5

Impulse

<II
c:

CII
QJ CII
2
c:
o C c:
N o
N 2 B
U
....
:::J
:.:;
Vl VI
S
CII "' "'
Z WJ c::

Position Set-up phase/"taking out the slack"

Time

Fig.2.29 Mobilization-with-impulse technique. Distance-time diagram.

20

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Treatment Principles of Various Manual Medicine Techniques

+y

�---X
----r-

-y
a b

Fig. 2.30a, b Neutral position of a spinal segment. Arrangement of the short and long rotator muscles.

Neuromuscular Therapy (NMT) muscles primarily responsible for motion and those re­
sponsible for posture. A rather powerful set of muscles is
NMT includes treatment procedures that improve mobility necessary to maintain the otherwise mobile head in posi­
and stretch a muscle by engaging direct muscle action andj tion.
or the associated neuromuscular reflex mechanisms (refer A well-founded knowledge of the functional anatomy is
to Dvorak and Dvorak, 1990). indispensable for proper neuromuscular treatment. Con­
Trunk rotation is affected by muscles oblique or even cerning the spinal areas, it is important to remember that
perpendicular to the longitudinal axis of the vertebral col­ rotation to one side is caused by the contralateral trans­
umn. This is primarily due to the action of the short and versos pinal system, while rotation may be typically limited
medium-length transversospinal muscles, especially the by the shortened ipsilateral transversospinal muscles.
rotator and multifidi muscles (Fig. 2.30). Significant trunk Rotation motion of the superior partner in the vertebral
rotation, however, requires the action of additional trunk spinal segment is initiated to the left, for instance, by the
muscles, such as the lateral abdominal muscles which con­ right rotator and multifidi muscles. Thus, the right rotator
nect the lateral aspect of the thorax with the pelvic crest on and multifidi muscles function as agonists for left rotation
the opposite side. The abdominal musculature introduces (Fig. 2.31). When the rotatores and multifidi muscles are
prominent flexion to the spinal column, which must be shortened in the same spinal segment, however, they di­
compensated for by the back extensor muscles. For the minish rotation to the right (Fig. 2.32).
neck muscles, one has to differentiate between those

21
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Definitions and Prindples of Manual Medidne Diagnosis and Treatment

Zl Z

X,

-y

a b

Fig. 2.31 a. b Spinal segmental rotation to the left.


'
x , Zl Motion barrier
+0y Rotation to the left of the superior vertebral joint partner
Red Activated rotator muscles-agonists for left rotation

Zl Z

X,

=-- .......-- x
IZ

-y

a b

Fig. 2.32a. b Pathologic motion barrier for segmental rotation to the right.
'
x , z' Pathologic motion barrier
+0Y Reduced left rotation (hypomobility) of the superior vertebral joint partner
Red Shortened rotator muscles which are the antagonists for right rotation-agonists for left rotation
IZ Irritation zone

22

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Treatment Principles of Various Manual Medicine Techniques

,
x

--�-------+--����--t---� x
IZ

-y

a b

Fig. 2.33a, b Pathologic motion barrier for se g me ntal rotation to the ri ght .
x', Zl = Pathologic motion barrier
+0Y = Pathologic segmental rotation to the left (left rotation hypomobility) of the superior vertebral joint partner
Red = Shortened rotator muscles which are the antagonists for right rotation
IZ = Irritation zone

• Since this type of movement is often new to the patient


NMT 1:
and at times difficult to learn, it may be of benefit to use
Mobilization Utilizing the Agonist Muscles
passive motion to guide the joint to the pathologic
Starting from the pathologic barrier, the patient contracts barrier.
the appropriate agonist muscles to mobilize beyond this • When teaching certain movements, it may be of benefit
barrier. The slack is taken up in the spinal segments next to to have the operator touch the skin overlying the par­
the restricted joints. Since it is often difficult for the patient ticular muscles that need to be contracted.
to learn these new movements, the operator can help both • This type of procedure is repeated several times in one
quantitatively and qualitatively by using palpatory assis­ session under supervision by the operator.
tance and verbal feedback to the patient. • The patient should also perform the movements rou­
NMT 1 teaches patients those mobilization techniques tinely on his own (Fig. 2.36).
that they can usually perform on their own in a home
exercise program.
The following considerations are of significance when
NMT2:
utilizing the NMT 1 technique:
Mobilization Utilizing the Postisometric Relaxation
Phase of the Shortened Muscles
• The restricted jOint must first be carried to its present
pathologic barrier (Fig. 2.33). If muscle testing reveals shortened tonic muscles then
• The segments distal to the restricted joints are fixated there will always be diminished associated regional or
(slack is taken up). segmental mobility in the corresponding spinal area(s) or
• The patient introduces some very slight movement be­ the peripheral joints (Fig. 2.33). Isometric contraction and
yond the pathologic motion barrier by contracting the subsequent stretching during the postisometric relaxation
appropriate muscle groups (Fig. 2.34). phase may return the muscles to their normal length. By
• Stepwise gain of movement (Fig. 2.35). engagement of the specific muscles, the corresponding
• Duration of sustained muscle contractions is typically joint or spinal segment is mobilized passively.
between 3 and 5 seconds.

23
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Definitions and PrInciples of Manual Medicine Diagnosis and Treatment

ziz' +y

X,
-0
y
I
- \ / -1= xix2

a <J=::l -y b

Fig. 2.34a, b Mobilization using NMT 1. +- = Direction of induced mobilization


x'. ZI = Pathologic motion barrier Red = Recruited rotation agonists
6. = Fixation of the inferior vertebra ZI Z2 x' x? = -elY = Mobility gain

AB PhysB

PB

Fig. 2.35 Stepwise mobility gain. Fig. 2.36 Self-mobilization technique to improve segmental right
AB = Anatomic barrier rotation.
PhysB = Physiologic barrier
PB = Pathologic barrier

The following considerations are of clinical significance • The muscle is subsequently stretched for 3 to
when utilizing NMT 2: 10 seconds during the postisometric relaxation phase
(Fig. 2.39).
• The incriminated muscle is stretched to near maximum. • Stepwise stretching: starting from this new position, the
Optimal isometric contraction is introduced, by the pa­ muscle is again stretched maximally and isometrically.
tient, away from the pathologic barrier (Fig. 2.37). • In most of the cases the patient needs to learn an in­
• The distal lying vertebra is fixated. dependent stretching home exercise program.
• Isometric relaxation of the incriminated muscle • In many cases, however. there is weakening of the
(Fig. 2.38). phasic muscles in addition to muscle shortening. and as

24

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Treatment Principles of Various Manual Medicine T echniques

l
Z Z

x,

--�---r-L-
---��-=�-r�---t--. x

IZ

-y
a b

Fig. 2.37 a, b Pathologic motion barrier for segmental rotation to the right.
x I, Z 1 = Pathologic motion barrier
+0Y Pathologic segmental rotation to the left (left rotation hypomobility) of the superior vertebra
Red = Shortened rotator muscles which are the antagonists for right rotation
IZ = Irritation zone

IZ

a +y -y b

Fig. 2.38a, b Isometric contraction.


l
Xl, Z = Pathologic motion barrier
6 = Fixation
-+ = Dire ction of is ometric contra ction
Green = Shortened right rotation antagonists which are isometrically contracted
IZ = Irritation zone

25
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Definitions and Principles of Manual Medicine Diagnosis and Treatment

X,

x/x'

a -y b

Fig. 2.39a, b Mobilization/stretching. Yellow Right rotation antagonists that are relaxed/
' ' stretched in the postisometric relaxation phase
x, z Pathologic motion barrier
6. Fixation in response to induced right rotation
Direction of induced mobilization/stretching Z® Z2 x, X2 -0Y Mobility gain

a rule the muscles should be stretched before being • The restricted spinal segment is guided to its pathologic
strengthened. barrier (Fig. 2.40).
• NMT 2 is most helpful in cases in which there is a soft • The restricted spinal segment or peripheral joint is fix­
end-feel with angular motion restriction. ated, thus barring further movement.
• The first step of treatment includes pure isometric
contraction in the direction of motion restriction (as­
suming correct fixation). This leads to a reciprocal in­
NMT3:
hibition of the shortened rotator antagonists.
Mobilization Utilizing Reciprocal Inhibition
• Duration of the isometric contraction is between 5 and
of the Antagonists
10 seconds (Fig. 2.41).
Isometric contraction occurs in the same direction as the • In the second step, careful passive mobilization is per­
motion restriction. The muscles antagonistic to those formed beyond the pathologic motion barrier (Fig. 2.42).
muscles that need to be relaxed are isometrically con­ This mobilization requires significantly smaller forces
tracted. With this technique, the incriminated segment is than those applied with the stepwise stretching proce­
the fixated. This is in contrast to the NMT 1 and NMT 2 dures during the postisometric relaxation phase of
techniques, in which the spinal segments that are above NMT 2.
and below the restricted spinal segment are fixated.
The following considerations are of clinical significance This technique is utilized when isometric contraction of the
when utilizing NMT 3: shortened tonic musculature is painful, a condition often
found with acute radicular syndromes.

26

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Treatment Principles of Various Manual Medicine Techniques

,
x

--�------�r-��-r�---t--'r-L- x

IZ

-y
a b

Fig. 2.40a, b Pathologic motion barrier for right rotation. Red Shortened rotator muscles which are the antagonists for
'
x , Zl Pathologic motion barrier right rotation
+0Y Pathologic segmental rotation to the left (left rotation IZ Irritation zone
hypomobility) of the superior vertebra

+y

IZ

a -y b

Fig. 2.41 a, b Isometric contractioll. Green Right rotation agonist muscles, which are isomet·
'
x , Zl Pathologic motion barrier rically contracted
6 Fixation IZ Irritation zone
t- Direction of isometric contraction

27
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DefInitions and Principles of Manual Medldne Diagnosis and Treatment

Zl +y

X,

xix'

-y
a b

Fig. 2.42a, b Mobilization/stretching. Orange = The right rotation antagonists that are reciprocally
f::, Fixation inhibited are being stretched
+- = Direction of induced mobilization/stretching x' x2 Z' Z2 = -0
Y = Mobility gain

Muscle Trigger Point Therapy • A myofascial trigger point is described as a hyperirrita­


ble spot, usually within a taut band of skeletal muscle or
While the primary objective of this section is to describe the muscle's fascia, that is painful upon compression.
the four major manual trigger point techniques, a brief gen­ Snapping type of palpation of the myofascial trigger
eral overview of the standard approaches to trigger point point usually induces a twitch response in the incrimi­
treatment is presented here. Travell and Simons (1983a, nated muscle.
1992) in their classic texts (both of which are comprehen­ • The patient usually reports pain or discomfort in an area
sive and superbly illustrated) describe a number of differ­ that is characteristic for a particular muscle. There may
ent techniques that can be utilized to treat and inactivate be reports of autonomic phenomena as well.
the various trigger points primarily concentrating on the • Muscles that harbor a myofascial trigger point are often
"spray-and-stretch" and the various injection techniques. shortened.
In clinical practice, and in particular when dealing with • Myofascial trigger points can be associated with dis­
seemingly "untreatable" chronic pain syndromes, the var­ eases that are identified with the structural Ie
. vel
ious approaches have been well received, albeit on an described in Chapter 2), with either systemic or local­
empirical basis. ized disorders or both.
The injections can be done by using a saline solution or a • Contraindications to treatment of a myofascial trigger
local anesthetic agent or utilizing a "dry needling" tech­ point must always be kept in mind, and such should be
nique (in which no substrate is actually injected). meaningfully integrated in the overall treatment plan.
The different manual techniques go hand in hand with • As the treatment may be painful, the operator should
the other trigger point treatment approaches as they di­ take the time to explain the procedures, their benefits
rectly address the potential connective-tissue reactions and potential side-effects, including pain.
and joint dysfunctions arising from the particular trigger
points (Table 2.4).
Manual Trigger Point Techniques
The following represents but a brief description of the
characteristics of the myofascial trigger points and their The manual approach to a myofascial trigger point includes
relevance in clinical practice: primarily four different techniques, which are described in
detail below (Dejung et aI., 2006).

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Treatment Principles of Various Manual Medicine Techniques

Table 2.4 Trigger point management considerations

Common Myofascial Trigger Point Treatments

• Spray and stretch technique


• Trigger point injections:
- Local anesthetic injections (e. g., bupivacaine, etidocaine, lidocaine)
- Steroid injections with local anesthetic (e. g., region of frozen shoulder
- Sterile water/saline injections
- Botulinum toxin injection
- Dry-needling
- Combination or stepped-sequence approach utilizing the above (e. g., local anesthetic injection series followed by
botulinum toxin injection to maximize time between injections with maximal improvement in functional abilities)
• Specific muscle stretching exercises after injections/or other treatment techniques
• Correction of underlying/associated biomechanical aberrations (e. g., correction of postural abnormalities, correction of
sacral-base unlevelness/short leg syndrome)
• Physical therapeutic management as part of the entire treatment approach rather than as passive, stand-alone treatment
(e. g., ultrasound, electrophoresis, electrical stimulation, biofeedback)
• Restoration of muscle balance (appropriate stretching, strengthening, balance, endurance, etc.)

Manual Treatment

• Specific manual treatment techniques: see this chapter for more details as well as Chapter 18.
• Various osteopathic manual medicine techniques may also be useful, especially when utilized In combination with appropriate
injections and/or active exercise regimens
• Specific techniques that might be useful include, among others:
- Articulatory techniques/high-velocity/low-amplitude techniques
- Balance-and-hold techniques
- Muscle energy techniques
- Myofascial release techniques
- Release-by-positioning techniques
- Soft-tissue release techniques (disinhibition, decompression techniques)
- Combinations of various techniques

Alternative/Complementary Techniques

• Myotherapy ("ischemic-stretching" technique; Prudden, 1980)


• Acupuncture treatment

Pharmacologic Treatment

• Examples of medications that might help, but should only be used judiCiously within a comprehensive evaluation and
treatment regimen that takes advantage of an active approach based on specific muscle involvement and particular
functional goals to be accomplished with the overall treatment approach):
• Muscle relaxants Oudicious use, if at all)
• Nonsteroidal anti-inflammatory medications Oudicious use, if at all)
• Tricyclic antidepressants

Technique I: Active Repetitive Contraction and Manual trigger point technique I is based on classical man­
Relaxation ual medicine approaches (Knott. 1968; Cailliet, 1977; Lewit,
The rationale behind the use of this treatment is the reduc­ 1981; Rubin, 1981). Trigger point technique I has been
tion of muscle tone in the muscie that harbors the myofas­ shown to be particularly useful in patients whose muscles
cial trigger point. The goal is to restore the original resting have become so shortened over time that they cannot be
length of the muscie by reducing its resistance to stretch. stretched to their normal resting length. This technique, in
Step 1: After exact and careful localization. the incrimi­ a sense, employs a "protective" mechanism of the muscle,
nated myofascial trigger point is carefully com­ as the pain will stop the patient from overstretching the
pressed. muscle. In performing the stretch under the supervision of
Step 2: The patient is requested to rhythmically contract the operator, the patient learns how to correctly stretch a
and relax the incriminated muscle that harbors the specific muscle, which is necessary if the independent
particular myofascial trigger point. home exercise program is to be successful. This also may

29
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Definitions and PrInciples of Manual Medicine Diagnosis and Treatment

foster the patient's confidence in the type of treatment ollr experience, should be typically 0.3 to 1.0 mL of injec­
rendered. tate per trigger point at any one time.

Technique II: Passive Muscle Stretch • Usually no more than six to eight different muscles
Step 1: Compression of the incriminated myofascial trigger should be injected per treatment session.
point after it has been carefully localized. • Maximally three to five injections into the same myo­
Step 2: The muscle that harbors the myofascial trigger fascial trigger point (over time), unless clinically indi­
point is passively stretched within the patient's cated. Good documentation about the particular muscle
pain tolerance. injected, immediate and follow-up response, any com­
Step 3: The muscle and fascial tissue surrounding the in­ plications, and initial and follow-up range of motion is
criminated myofascial trigger point are then ad­ essential.
dressed through a deep stroking type of massage. • Sufficient time between successive injection sessions,
with at least 3-4 days between sessions.
Technique III: Fascial Release • No more than a total of 15-20 mL of 1 % lidocaine per
Step 1: Compression of the incriminated myofascial trigger session.
point after it has been carefully localized.
Step 2: Application of the so-called "fascial release tech­ Associated Ultrasound Applications
nique," in which the fascia between muscle and Ultrasound treatment may be used as adjunct treatment in
skin is "freed up," resulting in easier displacement the presence of myofascial trigger points, and may be par­
of the fascia along the overlying skin. ticularly useful in the presence pain at the myotendinous
junction, enthesopathies, and peritendinopathies. Contra­
It is important that the particular myofascial trigger point is indications to ultrasound include malignancy and treat­
carefully localized by palpatory examination of the muscle. ment around fluid-filled cavities (e. g., the eyeball), near a
The palpatory pressure should be great enough to ensure pacemaker, a joint prosthesis, or a laminectomy site.
adequate treatment of the trigger point, on the one hand,
while at the same time one should be careful not to use Criteria and Goals for Effective Treatment
excessive pressure so as to avoid irritation of the surround­ • A high degree of manual skill is necessary (significant
ing tissues. amount of practice is necessary to gain the necessary
clinical experience).
Technique IV: Myofascial Release • A detailed medical and pain history and a careful ex­
("Fascial Separation") amination are the sine qua non of the initial assessment.
Step 1: Compression of the incriminated myofascial trigger The most appropriate diagnostic studies, if indicated,
point after it has been carefully localized. should be chosen: (1) according to the additional in­
Step 2: In a process similar to the one described for tech­ formation one expects to find; and (2) keeping in mind
nique III, manual trigger point technique IV utilizes whether any of the information thus gained would in­
the concepts of the "myofascial release" technique, fluence the specific treatment approach.
(originally an osteopathic manual medicine tech­ • Careful patient positioning often facilitates treatment.
nique). Here, the goal is to "separate" fascia from • The instructions given to the patient should be as spe­
muscle. While inherently using forces greater than cific as possible and should include a description of those
that required for manual trigger point technique III, activities and movements that should be avoided or are
the overall amount of force should be gauged ac­ expected to facilitate recovery (e.g., "do's and don'ts" as
cording to patient tolerance. well as specific supplementary stretching exercises).
• Treatment should be unhurried. Both patient and
therapist should be as relaxed as possible (not always as
Injection Therapy for Myofascial Trigger Points
easy as it may sound).
In the absence of definitive guidelines as to the exact • Specific treatment/management planning with periodic
intensity, frequency, and duration for trigger point injec­ monitoring should be based on objectively verifiable
tions, a common-sense approach is useful. Based on the goals (range of motion improvement, "muscle tension
fundamental work by Travell and Simons (1983a, 1992), signs," reduction in medications, ability to perform
and our own experience, the following approach is sug­ certain activities for longer periods of time, etc.) and
gested, always keeping in mind the patient's response and functionally meaningful medical "end-points" (activities
projected outcome based on objectively verifiable and of daily living, [ADLsj vocational and nonvocational ac­
functionally meaningful information. Each injection, in tivities, etc.).

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Treatment Principles of Various Manual Medicine Techniques

• The s pe cific trigger points. releva(lt clinical and (unc­ essary, a reconditioni(lg program should be accompanied
tional findings. overall clinical status. treatment, and by adequate pain treatment.
patient response should be adequately documented in The treatment goals, however, may be different for the
the medical record. patient and for the treating practitioner (Table 2.5):
• Specific goals, medical end points and parameters of
progress should be established by the practitioner in • Typically patients want their pain reduced or abolished
discussion with the patient. If there is insufficient as it may be affecting their overall well-being.
progress, the treatment should be continued, revised, or • The practitioner's goal is to reduce or eliminate the
terminated depending on the overall clinical situation. pain-associated nociceptive reaction in order to have
the patient return to as high a functional level as pos­
In clinical practice and in our experience, "unsuccessful" sible.
treatment can usually be ascribed to one of three factors or
to a combination thereof: If there are objective signs or indications of instability and/
or inadequate strength and endurance, referral should be
1. Wrong diagnosis. made to a qualified therapist (e.g., an experienced phys­
2. Inappropriate treatment. iotherapist) for a detailed assessment and treatment rec­
3. "Out-of-sequence" treatment: that is, areas other than ommendations including the most appropriate trunk
the painful/or treated area need to be addressed first. stability exercise program. The individual program is tai­
lored according to patient's pain level, functional status,
There may be additional factors that either have not been tolerance and motivation to participate in such a program.
clearly elucidated or take on a significance different from In general, such a program approach is divided into three
that which the clinical context would initially suggest (for phases.
instance: perpetuating factors, remote or recent trauma, In Phase I, the exercises should not cause any pain
patient motivation, and many others). whatsoever and should integrate the patient's usual ADLs
as much as possible. In Phase II, the exercises are "more
intense" than in Phase I and may just approach the patient's
pain threshold, but should not go beyond it. Only when the
Reconditioning and Training Therapy
patient has progressed to the point where pain and noci­
ceptive reactions are minimal or absent, is he or she able to
Pain; Nociceptive Reactions; Functional Deficits
enter the phase III of the program. The goal in this phase is
Within the field of manual medicine, two primary consid­ to train for maximal strength, muscular and aerobic endur­
erations determine the selection of a rational recondition­ ance, speed, and coordination.
ing program:

Muscle Function and Stabilization Exercises


1. The patient's pain and associated nociceptive reactions.
2. The impact the pain has on the patient's functioning. According to Bergmark (1989). the trunk muscles can be
grouped into two general categories: (1) the global (large­
The goal of a reconditioning program is to maximally im­ scale or "macro") muscles; and (2) the local (confined,
prove the patient's level of function. The type and intensity "micro") muscles, depending on their main mechanical
of a particular program are chosen according to specific properties in the stabilization-mobility spectrum of their
objectively verifiable and functionally meaningful data action (Table 2.5).
gathered in the detailed structural and functional evalua­ The large-scale or global muscle system comprises
tion. muscles that have a large cross-sectional diameter and
The nociceptive reactions associated with a patient's that produce large torque upon the trunk, spine, and pelvis
pain often reduce not only muscle strength but also affect without direct attachment. This group is then further div­
muscular and aerobic endurance and coordination as well. ided into those muscles that primarily act upon the
This can be objectively documented with an appropriately shoulder girdle and arm and those that act upon the pelvis
designed functional capacity evaluation, for instance, in and leg.
which the patient is requested to give his or her best effort. The local or confined muscles are those that attach
Depression, fear, and secondary gain issues, among others, directly to the lumbar spine and are primarily responsible
can negatively influence even the most carefully executed for segmental stabilization. These are the members of the
assessment, and therefore, the results of such tests must transverso-spinal system, namely the multifidi and rota­
always be interpreted with great caution. Whenever nec- tores muscles.

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Definitions and Prindples of Manual Medicine Diagnosis and Treatment

Table 2.5 The three phases of a reconditioning training program

Training Therapy Principles

Phase I Gravity The incriminated joint or region is usually Determine the position of the incriminated
Acute painful in certain positions, therefore one of joint or region at its present neutral position
the primary goals is to reduce ·stress" upon ("unloading")
the joint/region by unloading through careful
repOSitioning the joint to a nonpainful position:
• Supine position/side-lying
• Sling table
• Medicine ball
• Water buoyancy

Move­ Avoidance of exercises that cause pain: Determine in which direction the pain di­
ment • Isometric exercises minishes
• Dynamic slow exercises
• Isokinetic exercises

• low force or resistance ( 30% of maximal Emphasis is on an individually tailored ex­


force) ercise program
• High number of repetitions (20-30)

Phase II Move­ Allow exercises up to but not beyond pain Keep the nociceptive/painful reactions at a
Subacute ment tolerance: minimum while emphasizing the need to
• Dynamic slow exercises improve/maximize muscular balance
• Iso kinetic exercises
• 30-50% of maximal force or resistance
• 20 repetitions

Phase III Move­ Motion up to the motion barrier. Any compo­ • Make sure that nociceptive/painful reac­
Chronic ment nent of the training therapy can be utilized: tions are kept to a minimum, if there are
• Dynamic fast any at all
• DynamiC slow • Do not start with coordination/proprio­
• Resistive force between 30% and 90% of ceptive training components (i. e., back
maximum school training) unless Phase II has been
completed. It is virtually impossible to
adequately train coordination in the pres­
ence of pain due to compensatory move­
ments or pain inhibition
• When entering Phase III, modalities/appa­
ratus such as free-weights or strengthen­
ing machines can be added
• Take into consideration the patient's over­
all health status and particularly such
variables as the condition of the patient's
intervertebral disk, tendons, and ligaments
• To maintain the gains made (·steady­
state"), the training frequency should be
between 1 and 3 sessions per week

Movement of the head and neck in reference to the In Figures 2.43-2.67, the muscles that act to stabilize the
pelvis is accomplished by the large-scale muscle system, spine are depicted in green, while those muscles that act to
whereas the local muscles adjust or "fine tune" the asso­ induce motion are depicted in red.
ciated localized spinal motion with the primary goal of The complex three-dimensional motion patterns and
stabilization. The large-scale muscles are able to induce muscle actions have been analyzed and described by Kurt
spinal motion while the limbs are held stationary ("stabi­ Tittel, who coined the term "muscular chain" (Tittel, 2003).
lized"), or conversely they induce motion at the limb while The unencumbered interplay between agonists, synergists,
the spine is stabilized. and antagonists is required for unrestricted movement of
the variolls body parts in space.

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Treatment Principles of Various Manual Medicine Techniques

Functional Correlation between Various Muscles and Their Effect on the Trunk and Spine

Table 2.6 Muscle fu nctio n

M uscle Muscle Action When Trunk/Spine Muscle Action When Extremity is Stabilized
is St abi lized

Trapezius (descending portion) Elevation of shoulder • Side-bending of the neck

Sternocleidomastoid Inhalation • With neck extended: reclination (extension) of


(0-C2
• Unilateral contraction: side-bending, extension
and rotation to the opposite side

Pectoralis Adduction and internal rotation of • Trunk rotation


the arm

Latissimus dorsi Adduction and internal rotation of • Bilateral action: trunk flexion
the arm • Unilateral action: trunk rotation

Oblique abdominal muscles Valsalva maneuver • Bilateral action: trunk extension


• Unilateral action: trunk rotation

Rectus abdominis Valsalva maneuver • Trunk flexion

Quadratus lumborum Exhalation, Valsalva maneuver • Unilateral: trunk side-bending

Tensor fasciae latae Abduction of the thigh • Ipsilateral stabilization of hemipelvis or lifting/
raising of contralateral hemipelvis

Gluteus medius and maximus Hip extension • Flexion of the pelvis


• Decrease in lumbar lordosis'

Rectus femoris and sartorius Hip flexion • Extension of the pelvis


• Increase in lumbar lordosisa (i. e., ·swayback")

• Due to their insertion at the pelvic girdle . these muscles affect the lumbar spine indirectly. both statically and dynamically.

Cervical Spine Side-bending Motion

Shoulder Elevation

Fig.2.43 Shoulder elevation. Fig. 2.44 Side-bending of cervical spine. Fig.2.45 Inh a latio n motion.

33
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Definitions and Principles of Manual Medicine Diagnosis and Treatment

Latissimus Dorsi Muscle

Fig. 2.46 Depression of arms. Fig. 2.47 Side- bending of trunk. Fig. 2.48 Exhalation motion/coughing.

Abdominal Oblique Muscles

Fig. 2.49 Valsalva maneuver. Fig. 2.50 Trunk rotation.

Fig.2.51 Lumbosacral flexion (sit-ups with knees bent).

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Treatment Principles of Various Manual Medicine Techniques

Quadratus Lumborum and Tensor Fasciae Latae Muscles

Fig.2.52 One-legged stance. Fig.2.53 Side- bending at trunk and pelvis. Fig.2.54 Two-legged stance.

Gluteus Medius and Maximus Muscles

Fig.2.55 Hip extension.

Fig.2.56 Lumbosacral extension.

3S
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Definitions and Principles of Manual Medicine Diagnosis and Treatment

Iliopsoas Muscle

Fig. 2.57 Hip flexion-one-Iegged stance. Fig.2.58 Hip flexion at the trunk. Fig.2.59 Trunk and hip flexion (supine­
sitting).

Complex Muscle-Chains of the Trunk: Extension and Rotation

/j.

Fig. 2.60 Trunk extension and rotation. Fig.2.61 Trunk flexion and rotation­
standing.

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Treatment Principles of Various Manual Medicine Techniques

Trunk-Side- bending Movements This is important clinically. When the deep paraspinal
The deep paraspinal muscles of the back constitute the muscles are involved, even small loading forces may cause
fourth, and deepest, muscle layer and extend over one or exacerbate the patient's pain, a fact it is important to
spinal segment or only a few segments. Characterized by remember during the initial and second phases of a recon­
a relatively small cross-sectional area, they are usually ditioning program. This requires the judicious selection
innervated unisegmentally or plurisegmentally. While and execution of the various exercise components.
they "fine tune" the spine on a segmental level and/or a Thus, it is of paramount importance that the individual
specific spinal region, they do so in coordination with the exercise program be tailored according to each patient's
action of the other large muscles that act directly upon the specific and general needs. The appropriate exercise pre­
trunk and the spine. The deeper paraspinals can become scription dictates which muscle group(s) should be
very painful, especially when they are called upon to fulfill stretched and which should be strengthened, and at what
a "protective" function in which they attempt to limit point in time, with what frequency, and at what level of
("block") potentially abnormal segmental vertebral motion. intensity (Figs. 2.65-2.67).
The associated palpatory findings include increased muscle
tone ("spasms") and associated segmental hypomobility.

Fig. 2.62 Trunk side-bending-standing Fig.2.63 Trunk side-bending-standing; Fig.2.64 Trunk side-bending-standing;
initial side-bending motion. end- range to the left. end- range to the right.

37
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Definitions and Principles of Manual Medicine Diagnosis and Treatment

Fig. 2.65i1, b Phase I.


Extremity muscles, single and multiple
s egmental muscles.

iI L-_______ ______--', b

Fig. 2.66i1, b Phase II.


Oligo- and segmental muscles and
extremity muscles.

Fig. 2.67i1, b Phase III.


Oligo- and segmental muscles and
extremity muscles.

iI b

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Treatment Principles of Various Manual Medicine Techniques

Physical Therapeutic Modalities Heat Treatment


Heat when used in conjunction with manipulative proce­
When indicated and appropriately prescribed, physical dures is usually applied in the form of localized treatment
therapeutic modalities serve as a useful adjunct to the only, with the following effects:
various manual medicine procedures, the myofascial trig­
ger point treatments, and the training therapy program. • Increased soft tissue elasticity.
Within the context of this text, the primary goal of • Reduction of increased muscle tone ("spasm").
physical therapeutic intervention is to help reduce noci­ • Pain reduction (partial explained by the "gate-control"
ceptive reactions and thus pain. The various modalities are theory).
usually used for patient preparation before, or sometimes • Reduction of the viscosity of the tissues and synovial
after, the various manual medicine techniques (both the fluid.
impulse and non-impulse techniques) or in association
with the various trigger point treatment approaches. Contraindications to heat therapy include acute hemor­
Physical therapeutic modalities primarily address the rhage and inflammation, bleeding disorders, malignancy,
following symptoms and signs: insensate skin, and atrophic skin. Caution must be exer­
cised in patients who are pregnant or who have a signifi­
cant medical disease such as multiple sclerosis.
Table 2.7 Symptoms, signs, and possible physical therapeutic
modalities

Symptoms and Signs Treatment Modality


Electrotherapy
Acute pain Cold
TENS (Transcutaneous Electric Nerve Stimulation)
Subacute pain Heat. elec trotherapy . ultra­
sound The low-frequency impulses generated by a small portable
device (the TENS unit) are delivered via two to four electro­
Acute inflammation Cold
des applied over the patient's skin to reduce the patient's
Subacute inflammation Heat perceived pain. It is postulated that by stimulating the
Electrotherapy A-nerve fibers one is able to induce pain inhibition at the
Ultrasound
level of the medulla oblongata.
Increased muscle tone. Heat TENS units have been found more useful in acute than in
"hypertonic muscle" Classic massage chronic pain situations, and in particular when there are
Elec trotherap y
known anatomically identifiable sources such as an acute
Trigger point therapy
disk herniation or recent spinal fracture (due to osteopo­
Cr y otherapy ( nitrogen gas)
rosis, for instance, and often acute conditions).

Thermotherapy-Cold and Heat Treatments Treatments Using Low-frequency Current


(50-100 Hz) current treat­
The goal of these low-frequency
Cold Treatment ments is to reduce soft-tissue pain. While it is postulated
Localized treatment using cold modalities has the following that this form of treatment increases blood flow to the
effects: tissues, another explanation may in part be based on mech­
anisms described by the gate-control theory.
• Pain reduction through presynaptic inhibition of noci­ TENS and other forms of electrical stimulation are con­
ceptive transmission. traindicated in patients with advanced cardiac disease and
• Reduction in nerve conduction velocity. in patients with a pacemaker, because it may interfere with
• Reduction of increased muscle tone ("spasms"). the pacemaker's functioning. It should not be applied over
• Reduction of inflammatory processes. the eyes, carotid sinuses, or gravid uteri.

[n clinical practice, the application of cold as a treatment


Ultrasound Treatment
modality is usually restricted to the acute painful episodes
or nociceptive/pain reactions. Cold is contraindicated in the Ultrasound treatment uses sound waves between 0.8 and
setting of ischemia, insensate skin, severe hypertension, or 8 MHz. It can be quite useful for pain arising from the joint
cold sensitivity syndromes (e.g., Raynaud syndrome, cryo­ capsule. the myotendinous junction, and the tendons.
globulinemia). Some practitioners advocate the use of ultrasound as part
of preparation for myofascial trigger point treatment or

39
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Definitions and PrInciples of Manual Medicine Diagnosis and Treatment

manual medicine treatment in general. especially immedi- areas. or areas of acute infection. It should not be applied
ately before performing stretching techniques to a partic- over the eyes. or near a pacemaker. joint prosthesis. or
ular muscle or muscles. laminectomy site.
Ultrasound is contraindicated in patients with ischemic
tissue. acute hemorrhage. malignancies. anesthetized

Schematic Representation of the Various Treatment Modalities and Their level of Action

1 Cortex

[ 2 Thalamus
3 Reticular formation

2
Patient interview
Patient consent
Reassurance

Tranquilizer
Myotonolytica

Anesthesia. posterior root

----« Anasthesia. spinal nerve

'
-4
-_! J Anasthesia. peripheral nerve
PM T',2,] -< Anasthesia. joint receptor

Prostaglandin inhibitor

Trigger point therapy Mobilization with/without impulse


Massage
< Connective-tissue massage
Myotonolytica
Physiotherapy
Anasthesia. skin receptors;
electrotherapy (TENS)

Heat. cold

Fig.2.68 Schematic representation of the various treatment modalities in correlation with the level of application (adapted from H.D.
Wolff. 1980).

40

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3 Biomechanical Principles of the Spine and Joints

General Biomechanical Principles

yz
A weJl-founded understanding of spinal biomechanics is -- ---
helpful in the clinical and radiographic assessment and r-- - --1
treatment of tile spine and the limbs. This chapter is based
I I
I I
on the fundamental work by White and Panjabi (1978, I I
1990) and Panjabi (2003). It places particular emphasis I
I
I
on those biomechanical princi pies that are particularly I I
relevant clinically in the assessment of the various neuro­ I I
I I
musculo-skeletal (NMSK) disorders.
I I
Types of motion and the barrier concepts as related to I
I
I
the clinical practice of manual medicine have been de­
I I
scribed in the previous chapter. xz

Clinical Biomechanics of the Spine

The Axial System

Any movement in space can be defined within the frame­


work of a three-dimensional coordinate system. Derived
from general principles in the field of mechanical engineer­
ing, this system has also found general acceptance and ap­
plication in biomechanics, ensuring precise description and
definition of body movement or individual parts in space.
xy
The three-dimensional coordinate is based on the three
fundamental component axes constructed perpendicular
to each other. By convention, the human body in its neutral, Fig.3.1 Three-dimensional coordinate system.
anatomic position is placed in space, with the anteropos­ yz Sagittal plane

terior view being the standard examination view (Fig. 3.1). xz Horizontal plane
xy Frontal plane
The point of intersection (O-point) of the three axes is
hypothetically placed between the sacral horns. By con­
vention, a set of three reference arrows is arranged such
that they point in the positive direction, whereas arrows The combination of any two of the three axes defines one of
pointing in the opposite direction are, again by convention, the three major planes in this coordinate system (Fig. 3.1):
designated as negative.
The three primary axes are defined as follows (Figs. 3.1, • The sagittal plane is formed by the y- and z-axes.
3.2,3.3): • The horizontal plane is formed by the x- and z-axes.
• The frontal plane is defined by the x- and y-axes.
• The transverse (horizontal) x-axis. The direction to the
left from the center point is designated as +x, whereas This system then allows one to analyze any spinal motion

the direction to the right is designated as -x. in general, or a particular vertebral motion segment in
• The vertical y-axis, which is perpendicular to the x-axis. terms of rotation about a particular axis, or motion with
The superior direction is designated as +y, while the reference to or within a particular plane, or as a combina­
inferior direction is designated as -yo tion of different axes or planes.
• The sagittal z-axis, which is perpendicular to the x-axis In regard to axial rotation, clockwise rotation is desig­
in the horizontal plane. The anterior direction is desig­ nated as the positive (+) direction, whereas counter-clock­
nated as +z, whereas the posterior direction is desig­ wise rotation is designated as the negative (-) direction.
nated as -z.

47
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Biomechanical Principles of the Spine and Joints

,I t }
Foe"
III Load
Mom'"t

- T"nslation

Rotation
} Displacement

Fig.3.2 A three-dimensional coordinate system has been placed at forces or moments, can act on theses axes: the application of any
the center of the upper vertebral body of a vertebral unit (motion one of the load components (linear or rotatory) produces displace­
segment). An applied force (compression or distraction) or a rotary ment of the upper vertebra with respect to the lower vertebra. This
moment (along an axis either clockwise or counterclockwise) sub­ displacement consists of translation and rotation. With permission
stitute a loading force that will result in displacement of a vertebra. from White and Panjabi, Clinical Biomechanics of the Spine, Lip­
A total of 12 load components, that is either linear or rotatory pincott Williams & Wilkins, 1990.

• Flexion (+0X) describes positive rotation around the x­ Using this convention, it is possible to break down the more
axis in the sagittal plane. complex movements into individual uniformly defined
• Extension (-0X) describes negative rotation around the movement components. In other words, any movement
x-axis in the sagittal plane. can be described as a function of a rotational movement
• Side-bending (lateral bending) to the right (+0Z): positive around a particular axis. Clockwise rotation is designated
rotation around the z-axis in the frontal plane. as +0, and the counterclockwise rotation is designated as-0
• Side-bending (lateral bending) to the left (-0Z): negative (Fig. 3.3).
rotation around the z-axis in the frontal plane. Side-bending movement to the right is described as
• Axial rotation (+0Y), positive rotation to the left around rotation +0Z, while side-bend ing to the left corresponds
the y-axis in the horizontal plane. to the description of -0Z. Forward flexion motion in the
• Axial rotation (-0Y), negative rotation to the right sagittal plane corresponds to +0X, and spinal extension is
around the y-axis in the horizontal plane. denoted by -0X. Axial rotation to the left is described by
+0Y, whereas rotation to the right corresponds to -0Y.

42

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Clinical Biomechanics of the Spine

/
/ -<
/
/
/
/
/
/
Y

I
I
I
I
I
I
I
I-y
t
Fig.3.3 Three-finger model applied to the three-dimensional coordinate system.

Other Motion Description Conventions • Motion between two adjacent vertebrae (the two part­
ners of a spinal segment, also called the vertebral mo­
In recent years, additional conventions have been intro­ tion unit or motion segment) is described by convention
duced to further assist in establishing a "common lan­ as movement of the superior partner of the two verte­
guage" for the description of both gross spinal motion brae in relationship to its inferior vertebral partner.
and individual segmental movement: • Degrees of freedom: Each spinal facet joint has six
degrees of freedom. This is in contrast to the six motion
• Vertebral rotation around a particular axis is defined in directions just described above (flexion-extension,
reference to the superior or the anterior portion of the side-bending left and right, axial rotation left and right).
particular vertebra (Fig. 3.4). For example, axial rotation Each degree of freedom, based on motion in relation to a
of the vertebra to the left (+I1lY) denotes that the anterior particular axis, is defined in terms of: (a) motion about/
aspect of the vertebral body moves to the left direction. around one axis (rotation); and (b) motion along an axis
(translatory motion).

43
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Biomechanlcal PrInciples of the Spine and Joints

Thus, rotation about and translation along the x-axis for


y
instance would define two degrees of freedom in rela­
tionship to the x-axis. This can be applied equally to the
other two axes, giving six degrees of freedom for all
three axes.

Although individual physiologic movement components


should, in theory, be amenable to a well-defined analysis
using the descriptive mathematical-mechanical model, it
x "
should always be remembered that the vertebral column is
both anatomically and functionally a rather complex sys­
tem that simultaneously has to fulfill dual roles-namely,
assuring sufficient stability while at the same time allowing
sufficient motion.
Movement in the individual spinal segments is a combi­
nation of translatory and rotatory movements around a
particular axis as defined by the three-dimensional coor­
dinate system (refer to Fig.3.2). (5
x 11;;.

Coupled Motions

Axial rotation (±0y) and side-bending (±0Z) in a spinal seg­


ment usually do not take place in a single motion direction
in a "pure" plane type of motion, as these two movement
directions are coupled to each other. This linkage has be­
come known as coupling patterns (Lysell, 1969; White and Fig. 3.4 Definition of rotation movement.
Panjabi, 1978, 1990; Stoobey, 1967).
The individual coupled motions are governed by the
architecture of the vertebrae (smooth, rough, etc.), their
joint surface inclination, the associated ligaments, and the
interactive functioning of the paraspinal muscles. The
physiologic anteroposterior curvature of the spine in the
sagittal plane is of great significance as well.

Biomechanics of the Upper


Cervical Spinal Joints (CO-(1-(2)

Atlanto- Occipital Joint (CO-C1)

The articulation between the skull and the atlas is formed


by two paired structures, each of which consists of the
occipital condyle and the superior facet of the atlas. The
articulating surfaces are oval, resembling a beanlike con­
figuration. The upper surface of the condyles is convex,
while the surface of the superior facet of the atlas is con­ Fig.3.5 Sagittal angle of the joint axes for the OCCipital condyles
cave. In the adult, the sagittal axial angle of the joints (after Ingelmark, 1947).
1 Occ ip ita I condyles
measures between 50° and 60° (Ingelmark, 1947; Bernhard,
2 Foramen magnum
1976) (Fig. 3.5).

44

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Biomechanics of the Upper Cervical Spinal Joints (CO-Cl-Q)

t l··

Fig.3.6 Frontal angle of the jOint axes for the occipital condyles
(after Stoff, 1976a) is 124' for men, 127' for women (blue: artic­
i.t1 :' ::
:
"

('i'
" :

'
..
..
ulating surface). .\3 .

The frontal axial angle of the joints (Fig, 3.6) results from
lines drawn parallel to the articulating surfaces of the con­
dyles. On the average, it measures 1 24.2° (Stoff, 1976). This
axial angle is increased in the presence of condylar hypo­
plasia and basilar impression.
Von Lanz and Wachsmuth (1979) describe the joint
between the occiput and the atlas as a modified spherical
articulation, with motion taking place around two axes
according to the anatomic arrangement. The left and right
joints actually appear to function with greater motion
F ig .3.7 Axes of motion of the occipito-atlanto-axial and cervical
around the transverse axis than the sagittal axis.
joints. (After Knese, 1947.)
Flexion and extension movements take place around the
transverse axis, whereas side-bending is around the sag­
ittal axis (Fig. 3.7).

Function of the Upper Cervical Spinal JOints (CO-C1) Table 3.1 Li mi tati on of range of motion about the transverse axis in
the upper cervical spinal joints
At the atlantoaxial articulation, rotation takes place around
the transverse axis, measuring an average of 240• It is Flexion (Inclination) Extension (Reclination)
limited by the bony and surrounding soft-tissue structures
Nuchal ligament Bony structures
(Panjabi et at. 1988; White and Panjabi 1990) (Table 3.1).
Alar liga ments Anterior neck muscles
Rotation about the transverse at this spinal level has been
specifically termed inclination and reclination motion, Anterior longit udinal
analogous to forward nexion and extension, respectively, ligament
Cervical spine nexion takes place in two stages (Oul,
1982; Arlen, 1977; Gutmann, 1981). During the first stage,
only a positive rotation around the x-axis in the CO-C1
Alar liga m e nt s
spinal segment has been observed, This forward movement
of the head in relation to the atlas is approximately 80, Posterior neck muscles Anterior longitudinal
ligament
which has also been assigned the speCific term of nutation
motion ("nodding"). The spinal segments below this point Lig amentum f1avu m
remain in the neutral position. (res t rains hyperflexion)
It is not until the second phase that rotation (+0X) takes
place in the remaining cervical spinal segments below
CO-C1: C1-C2 is tilted forward; C2-C3 to C6-C7 undergo
flexion. The axis rotates 450 with respect to C7.

45
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Biomechanical Principles of the Spine and Joints

t
y '

v . y'

'I .

I
--
x -- - - -- ,-
I
tt- - - ---

m
I
Fig.3.8 Gliding movement of the atlas with side- bending to the right.

Furthermore, during this second phase a positional spine. Lewit's (1986) findings vary from those reported by
change occurs in the CO-C1 segment at the same time as Werne and Fielding, while Gutmann (1985) and Kamieth
the head rotates backward (in relation to the atlas). This (1987) emphasize that there is virtually no atlas rotation
relative negative rotation of the head with reference to the with pure side-bending movement.
atlas and the axis (i. e., backward rotation) prevents exces­ Various mechanisms have been proposed to explain the
sive cervical spine extension (e.g., avoiding an abnormal cause of this forced rotation. Most authors agree that it is
kyphotic component) thus preventing potentially adverse due to the unique anatomic architecture of these articula­
position of the spinal canal. tions in the cervical spine.
Side-bending, also commonly referred to as lateral bend­ Werne (1957) suggests that the forced rotation of the
ing, takes place around the sagittal axis and amounts to axis is the result of the eccentric insertion of the alar
approximately 5° to either side (Panjabi et aI., 1988; White ligaments. Jirout (1973) postulates that, in addition to the
and Panjabi, 1990; Penning 1976). It is greatest when the influence of the articular processes, the muscles in the head
head is slightly flexed and is reduced due to the function of and neck region with their insertions at the spinous pro­
the alar ligaments. cesses play a specific role in achieving forced rotation dur­
With side-bending, Gutmann (1981) reports a trans­ ing the second phase.
verse gliding movement of the atlas between the condyles In the atlantoaxial joint, in addition to axial rotation,
and the body of the axis (in the atlanto-occipital and at­ there is displacement of the atlas in the same direction as
lantoaxial articulation). The gliding movement occurs in side-bending (in the frontal plane). This becomes apparent
the same direction as the gross side-bending movement on the anteroposterior radiographic view, where the dens
(Fig. 3.8). of the axis is located asymmetrically, on either side of the
Reports published in the literature that have investi­ center between the two lateral masses. The offset is termed
gated the biomechanics of side-bending movement at positive when the surface of the atlas projects beyond the
CO-C1 have also not been consistent. Pure cervical spine surface of the axis, and is negative when the surface of the
side-bending motion without simultaneous rotation of the axis projects beyond that of the atlas. Furthermore, the
head would indeed represent a rather biomechanically appearance and degree of offset are dependent upon the
complex movement. In addition to segmental tilting, there changes stemming from the rotation of the axis itself.
is always forced coupled rotation in the same direction as According to Gutmann (1985) and Lewit (1986), it is the
that of side-bending in the C2-C7 vertebrae. Starting at the wedgelike anatomic arrangement of the atlas that causes it
superior end of the cervical spine, the degree of this forced to be displaced toward the side of lateral bending.
rotational movement decreases in the inferior direction. Reports about the lateral displacement of the atlas have
Werne (1957) and Fielding (1957) report that with maximal been equally inconsistent. Keim (1953) found that with
side-bending the axis actually rotates to a greater degree maximal side-bending, lateral atlas displacement occurred
than during maximal rotation of the head and cervical in all of the 25 cases studied. Lewit (1986), studying a group

46

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Biomechanics of the Upper Cervical Spinal Joints ((o-0-C2)

of 30 healthy persons. found in four cases a paradoxical


lateral atlas displacement; that is. where the atlas was Anterior
displaced toward the side opposite to that of lateral bend­
ing. In both of these studies, the side-bending motion was
introduced actively by the study participants.
Jirout (1973) found that atlantoaxial movements are
more pronounced during passive than during active side­ -+--+---'-- 2
bending motion. Kamieth (1986) postulates that the dis­
placement is due to induced or forced motion at the axis.
'r---3
We hypothesize that the lateral atlas displacement may
actually result from engaging the anterior portion of the Left Right

alar ligament as it wraps itself around the dens. Assuming


the course of the alar ligaments follows that described by
Ludwig (1952), our hypothesis for the lateral atlas displace­
ment also postulates that the lateral displacement is sec­
ondary to the forced rotation of the axis (Fig. 3.9). -+--+--'--- 2
In all of the 30 adolescents studied by one of the authors
(Reich and Dvorak, 1986a,b) the gliding movement of the "r-""'--- 3
"
atlas occurred in the same direction as the induced side­
bending motion. This gliding movement became even Posterior
more pronounced in patients with demonstrated atlan­
toaxial instability secondary to rheumatoid arthritis. The Fig. 3.9 Atlas displacement with side-bending; hypothetical mech­
distance between the dens of the axis and the lateral mass anism. Coupled rotation of the axis causes the anterior portion of
of the atlas was used for measurement. the right alar ligament to be wrapped around the dens, thus bring­
ing the right-sided lateral mass of the atlas closer to the dens. The
Not surprisingly, reports about the rotation movement in
anterior portion of the left alar ligament does not become tight
the atlantoaxial joint are also not consistent. Fielding
until its insertion has been rotated into the posterior position.
(Fielding, 1957; Fielding and Hawkins. 1978), White and (After Werne. 1957.)
Panjabi (1978). and Penning (1968) reported that rotation 1 Alar ligament
in this joint is nonexistent. whereas Depreux and Mestdagh 2 Dens of the axis
3 Atlas (lateral mass)
(1974) described approximately 5° of motion. with values
being significantly higher in persons who had undergone
atlantoaxial fusion.
three-dimensional motion patterns in the upper cervical
Gutmann (1981) reports that when the head is turned,
spine. It was found that the atlanto-occipital rotation mea­
both the head and atlas rotate simultaneously (±0Y) with
sures 7° to either side. Table 3.2 summarizes the mean
respect to the axis. The lateral portion of the fibrous joint
range of motion values at the atlanto-occipital articulation
capsule associated with the facet joints in the upper cer­
as presented by various investigators.
vical spine is taut, allowing for particular control of rotation
and side-bending, in conjunction with the other limiting
anatomic factors, namely, that of facet joint inclination.
Caviezel (1976) clinically utilizes a so-called "springing Atlantoaxial Joint ((1-(2)
test" to assess passive rotation at the extreme of opera­
tor-induced rotation. The atlantoaxial articulations are of great clinical signifi­
Using functional computed tomography (CT) scans of cance in the field of manual medicine. Here, motion takes
the upper cervical spine in fresh cadavers, rotation be­ place within four articular spaces, one of which is desig­
tween the occiput and the atlas was unequivocally demon­ nated as the atlantodental bursa and is represented by the
strated (Dvorak and Hayek, 1986) with reported mean space between the transverse ligament of the atlas and the
values of 4.5° and 5.9° for rotation to the right and to the dens of the axis.
left. respectively . In healthy adults, rotation between the The medial atlantoaxial joint is located between the
occiput and the atlas was also clearly demonstrated via dens of the axis and the posterior surface of the anterior
functional CT scans, with an average value of 4° (Dvorak arch of the atlas. The two articular spaces of the lateral
and Hayek, 1987). atlantoaxial joint are of particular importance (Fig. 3.10).
The in-vitro studies by Panjabi et al. (1988) and Crisco et The joint surfaces are usually round. but sometimes
al. (1991) utilized stereophotogrammetry to evaluate the triangular, and are covered with cartilage that is 1.4 to

47
Copyrighted Material
Blomechanlcal Principles of the Spine and Joints

Table 3.2 Range of motion at the occipitoatlantal (OA) joint according to various authors


Author Flexion/Extension (Total) Side- bending Axial Rotation l/R
(lateral Flexion) l/R

Fick 1904 50 30-40 0


--_..
- -------
_-

Poirier et al. 1926 50 14-40 0


-- -=......:::-.-.. -
Werne 1957 13 8 0
.-=-=-�-
-
Depreux et al. 1974 5
= --- --- -
Penning 1978 30 10 0
- �=.-=-=� - .-
Dvorak et al. 1985 5.2

Clark et al.
--
1986 22.7
-
-== =I__

[ -'
...JL.- _______ .--- - . ..
.
__
.
..

4.8
-

11-
-_.

Dvorak et al. 1987 4


-. �.=...-
....:.. =
Penning et al. 1987

Panjabi et al. 1988 24.5 5.5 7.2


Dumas et al. 1993

a b

Fig.3.10
a Atlas. superior view; the superior joint surfaces are oval. some-
times with double formation (right).
b Atlas . view from inferior; round joint surfaces.
c Axis. superior view; the joint surfaces point inferiorly (convex).
1 Transverse process
2 Anterior tubercle
3 Superior articular facet of the atlas
4 Transverse foramen
5 Posterior tu bercle
6 Inferior articular facet of the atlas
7 Spinous process

3.2 mm thide The articular surfaces of the axis are convex. The joint capsule is wide and flabby. and from the me­
and those of the atlas are relatively flat. causing an anterior dial wall a cuneiform synovial fold invaginates into the
and posterior gap of 2-5 mm (Knese. 1947) (Fig. 3.11). articular space. which is described as meniscoid (Dvorak
and Aebi. 1987).

48

Copyrighted Material
Biomechanics of the Upper Cervical Spinal Joints (CO-C1-C2)

Function of the Atlantoaxial Joint

Flexion and Extension


The bony structures of the articular surfaces and the mo­
tion-limiting ligaments allow movement around the trans­
verse axis that can be as large as 10° and 15° (Figs. 3.10.
3.11). Using lateral radiographic projections. the effective­
ness of the ligaments can be determined by measuring the
distance between the posterior portion of the anterior arch
of the atlas and the dens of the axis.

Side-bending
Side-bending between C1 and C2 is only possible with Fig.3.11 Paramedian sagittal section of the upper cervical spine.

simultaneous rotation around the axis. This is described 1 Occipital condyle


2 Atlas
as forced rotation and is thought to be the result of the
3 Axis
physiologic function of the alar ligaments. Lewit (1970) and
4 Vertebral artery
Jirout (1973) report displacement of the atlas in the same 5 Great occipital nerve
direction as that of the forced induced Side-bending. 6 Meniscoid

Axial Rotation
62 3 4
The head and atlas rotate simultaneously on the axis
around the dens. The axis of rotation passes through the
dens of the axis and is clinically "secured" by the transverse
ligament of the atlas (Fig. 3.12). Average rotation in the
young. healthy adult is 43° (SO = 6°). which amounts to
approximately half of the total cervical spine rotation
(Dvorak and Hayek 1987).
Normal values for axial rotation in the upper cervical
spine are listed in Table 3.3.
Cinematographic studies by Fielding (1957.1978) clearly
demonstrate that. starting with the head in the anatomi­
cally neutral position. head and cervical spine rotation
occurs first in the atlantoaxial joints. Once their motion is Fig.3.12 Schematic representation of the ligamentous apparatus
completed. the lower cervical spine segments can begin to at the craniocervical junction.

rotate. The limitation of the rotation is primarily deter­ 1 Atlas


2 Dens of the axis
mined by the alar ligaments (Figs.3.n. 3.14).
3 Atlantal portion of the alar ligament
4 Occipita l portion of the alar ligament
Coupled Movement 5 Transverse ligament of the atlas
• Motion between segments is primarily a coupling be­ 6 Anterior atlantodental ligament

tween that in the frontal plane (±0Z) and the transverse


plane (±0y). This may occur in either two or three di­
mensions. According to Gutmann (1981). axial rotation
of the head (±0y) and atlas rotation in the opposite movement. Axial rotation is accompanied by a vertical
direction occur with side-bending. while C2 undergoes translatory gliding movement (y-axis). The literature
axial rotation toward the same side as in side-bending. relating to the motion of the atlantoaxial joint is sum­
• Translatory gliding: Minimal lateral translatory gliding marized in Table 3.3.
of up to 2-3 mm takes place in the sagittal plane (z-axis)
and the transverse plane (x-axis) (Hohl. 1964). These
two movements are always coupled to axial rotation

49
Copyrighted Material
Biomechanical Principles of the Spine and Joints

Table 3.3 Range of motion at the atlantoaxial joint according to various authors

Author Side- bending lateral Axial Rotation L/R


Flexion (unilateral)

Fick 1904 0 0 60
-- -- - -�- ==-==-=---=� --

Poirier et al. 1926 11 30-80


-=-- - -- -- - -- - --
Werne 1957 10 0 47
:::- -:-='---- -= :
Penning 1978 30 10 70
Dvorak et al. 1985 32.2
-- . --.
Clark et al. 1986 10 14.5
-- -- -- - --
Dvorak et al. 1987 43.1
- --=- -=-==-=----=-"=--=...
-: =
Penning et al. 1987 40.5
--
- - --_.
- - -- - - .- --
Panjabi et al. 1988 22.4 6.7 38.9
- - -- _.-

Dumas et al. 1993 37

j)jJ.
. :.::.:.. . ; ;
":' ':' '.:!'v

')
l

a IL________ _____ ______ ______ __


I\ '
1)/1 'r{I b

Fig.3,13a-c The alar ligaments. seen (a) from superior and (b)

'•
...

I..
from anterior, (After Ludwig, 1952,) c Anatomic specimen in the
., . anteroposterior view_
"
1 Left alar ligament
2 Dens of the axis

--:- :.-
.
3 Right alar ligament
4 Longitudinal ligament

.' .:
. : :
,. , 'I", , < ':; " -
-.
....' '. , 'i • •

.
,
',
' ,
..
.,. '. " - ,,
-
-"
" t1!I ';"
."
, •
-

• . It J\ 'i' !' ' . ..... '.


'fI
.

'f . "'- ,
,
.
• . • . -

c \ "-
..."f , Al q,t. ;. .

50

Copyrighted Material
Biomechanics of the Upper Cervical Spinal Joints (CO-Cl-C2J

Ligaments of the Upper Cervical Spine (CO-C1


and C1-(2)

The ligaments that are of particular interest with regard to


the function of the atlanto-occipital and atlantoaxial joints
are the alar ligaments and the cruciform ligament of the
atlas (Fig. 3.12).

Alar ligaments

Ludwig (1952) describes the alar ligament as an irregular,


quadrilateral pyramid-like trunk. The rectangular base lies
against the supenor two-thirds of the lateral surface of the Fig.3.14 Ligamentous interconnection between the dens of the
dens. The superior, posterior. and anterior surfaces connect axis and the atlas. View from superior onto the ligaments associ­
ated with the upper cervical spinal joints. The probe is on the
the dens with the occipital condyle, while the inferior and
anterior atlantodental ligament.
lateral surfaces connect the dens with the lateral mass of
1 Anterior arch of the atlas
the atlas (Fig. 3.13). 2 Anterior atlantodental ligament
The orientation of the fibers in the sagittal plane is 3 Alar ligament
primarily a function of the height difference between the
tip of the dens of the axis and the occipital condyles
(Fig. 3.13). The ligament that connects the dens of the axis
with the anterior arch of the atlas is part of the alar liga­
ment as well (Fig. 3.14). Occasionally, the presence of an­
other ligamentous connection between the base of the
dens of the axis and the anterior arch of the atlas has
been reported, and has been referred to as the anterior
atlantodental ligament.

Biomechanics of the Alar ligaments


The mechanical properties of the alar ligaments depend
primarily on three factors:

• Fiber orientation.
Fig.3.15 The alar ligaments are made up of collagenous fibers
• The proportion of collagenous versus elastic fibers.
(Giemsa stain).
• The mechanical properties of the collagenous and elastic 1 Dens axis
fibers. 2 Left alar ligament
3 Right alar ligament

The collagenous fibers will be irreversibly stretched if sub­


jected to a stretch beyond 6-8% of their resting length, and
will ultimately start to tear when stretched beyond that Function of the Alar ligaments
limit (Abrahams, 1967). Elastic fibers, in contrast, can be The function of the alar ligaments can be straightforwardly
stretched to 200% of their resting length, beyond which, inferred from their course by following them from their
however, they will rupture abruptly. It can thus be said that attachment at the occipital condyles to that at the atlas. The
ill essence the collagenous fibers do not undergo any per­ p rimary role of the alar ligaments is to limit axial rotation
ceptible stretch. in the upper cervical spine, particularly at the (0-C1 and
The alar ligaments are made up almost entirely of col­ (1-(2 articulations. Rotation to the right is limited by the
lagenous fibers (Fig.3.1S). At their attachments they run left alar ligament and, conversely, rotation to the left is
parallel, while at the center they tend to be interdigitated limited by the right alar ligament. Rotation to one side
in a criss-cross pattern (Dvorak et aI., 1988a). Saldinger et causes the contralateral ligament to become more taut
al. (1990) report that the alar ligaments begin to tear at 200 (Fig. 3.16). During side-bending motion toward one side
newtons. ( = rotation around the z-axis), the occipital portion of the
ipsilateral ligament is relaxed whereas the atlas portion

51
Copyrighted Material
8Iomechan/cal Prlndples of the Spine and Joints

z + oy

x x x

Fig.3.16 Function of the alar ligaments during rotation in the atlantoaxial joint ((1-(2).
z-z ' Rotation to the right y-y ' Side-bending to the right
z-z " Rotation to the left y-y" Side-Bending to the left

-oz y + oz
y

'
-x

/ / I,
\ C2
/
4J
Lv. Oy -o

Fig.3.17 Function of the alar ligaments during side-bending in the atlantoaxial joint ((1-(1).

becomes taut. This mechanism then limits the gliding mo- the same direction as the convexity (Fig. 3.17) (Reich and
tion of the atlas in the same direction as the induced side- Dvorak, 1986; Dvorak and Panjabi, 1987b). Despite a num-
bending movement. At the same time, the occipital portion ber of experimental studies, it cannot be conclusively
of the opposite alar ligament becomes tighter, which limits stated whether the alar ligaments are alone responsible
gliding of the occipital condyles in the opposite direction for the described forced rotation of the axis. This is espe-
(Fig. 3.17). cially true since the joint architecture and in particular the
The tight occipital portion of the alar ligament with its surface inclination, may play an inherent role. More studies
posterior and eccentric origin at the dens of the axis, to- are necessary to clarify the complex function of the alar
gether with the atlantal portion and its anterior eccentric ligaments.
origin at the dens, induces forced rotation of the axis in the Flexion in the upper cervical spine is chiefly limited by
same direction as the side of induced side-bending. Clin- the nuchal ligaments, the posterior longitudinal ligaments,
ically, and according to the convention of motion descrip- the tectorial membrane and the longitudinal fascicles of the
tion using the anterior portion of the vertebral body as the cruciform ligament. Increasing tension in the alar liga-
reference, the spinous process of the axis moves oppositely ments as the spine gradually moves toward the extreme
to the induced Side-bending. In other words, it moves in

52

Copyrighted Material
Biomechanics of the Upper Cervical Spinal Joints (CO-C1-C2)

of exion also participates in the limitation of nexion (Pan­


jabi et al.. 1991 ).
The alar ligaments are subject to great tension forces
and are therefore more likely to be irreversibly stretched or
may ultimately rupture. This is especially true in a situation
where the head is rotated maximally (rotation around the
y-axis) followed by nexion and extension movements (ro­
tation arollnd the x-axis). A similar position has been ob­
served in people involved in rear-end motor vehicle colli­
sions. It can therefore be surmised that under similar cir­
cumstances it is the alar ligaments that are subject to
damage. whereas the transverse ligament might remain
unaffected.
During rotation motion of the atlantoaxial joint. the alar
Fig.3.18 Prepared specimen at the transverse ligament of the atlas
ligament on the opposite side is stretched and "rolled up"
between the articular process of the atlas.
arollnd the dens of the axis; the alar ligament on the same
side relaxes. Thus. during rotation to the right. the left alar
ligament is wrapped around the dens while the right liga­ Function of the Cruciform Ligament of the Atlas
ment is relaxed (Figs. 3.9.3.16). The function of the cruciform ligament is to regulate and
During Side-bending motion, the ipsilateral alar ligament limit physiologic rotation between (1 and (2 and to protect
relaxes. and the stretched ligament of the opposite side the spinal cord form the dens of the axis.
causes a forced rotation of the axis in the direction of the
bending. due to its attachment to the dens of the axis. In the
Injury to the Ligaments Associated with the
clinical examination. the spinous process of the axis rotates
Upper Cervical Spine (CO-C1, (1-C2)
contralaterally (Fig.3.17). Thus. the strong alar ligaments
are able to limit the rotation motion of the atlantoaxial The transverse ligament of the axis ruptures at approxi­
articulation (Panjabi et al.. 1991). mately 350 N. Histologic examinations reveal that the pri­
mary site of rupture is at the bone-cartilage insertion inter­
face (Saldinger et al.. 1990).
The Cruciform Ligament of the Atlas
Macalister (1893) found that the transverse ligament of
The cruciform ligament consists of two differently directed the atlas tears at a load of 1275 N (130 kg). Fielding et al.
components: the horizontal transverse ligament of the (1974) examined the tensile strength of the alar ligaments
atlas and the vertical longitudinal fasciculi (Fig. 3.18). The and the cruciform ligament of the atlas in 20 corpses. They
transverse ligament of the atlas arises from the medial found that theses ligaments tear at a load of 400 N to
surfaces of the lateral masses of the atlas. while some fibers 1800 N (average. 1100 N).
also attach to the tip of the dens. In its central portion. the The transverse ligament of the atlas tears when
cruciform ligament is approximately 10 mm high and stretched beyond a length between 4.8 and 7.6 mm. Over­
2 mm thick and is covered by a thin layer of cartilage. The stretching will lead to tearing of the collagenous fibers.
lo ngitudinal fascicles are comparatively weak and are which is represented on radiographs as an increase of
present inconsistently. They merge with the atlanto­ more than 3 mm between the dens and the posterior sur­
occipital membrane (Saldinger et aI., 1990). face of the anterior arch of the axis (more prominent in
radiographs taken in the flexed position). When there is an
Biomechanics of the Transverse Ligament of the Atlas increased distance of 7 mm, complete separation of the
The transverse ligament of the atlas consists primarily of transverse ligament from the atlas should be suspected.
collagen fibers that may become irreversibly stretched while distances greater than 10-12 mm would be a clear
when subject to excess tension (Kennedy et aI., 1976). The indication of a torn alar ligament.
collagenous fiber bundles are oriented in parallel at the The spatial relationship between the bony structures of
insertion only to form a criss-cross pattern at the center the atlas. the dens of the axis. the spinal cord. and the free
of the ligament. which is also the thickest portion. The zone is designated as an anatomical constant. Generally,
portion facing the dens of the axis may reveal fibrocarti­ the rule of "thirds" due to Steel (1968) has proved valuable
lagenous changes. (Fig. 3.19). One-third of the space is occupied by the dens,
one-third by the spinal cord, and one-third by a free space,
the so-called safety zone of the spinal cord.

53
Copyrighted Material
810mechanlcal Principles of the Spine and Joints

Considering the significance of the anatomic position of


the cardiac and respiratory centers in the medulla oblon­
gata, it is plausible to hypothesize that there are not one

ZJ ""· ·t p
. but two sets of ligaments that assist in the prevention of a
I 1'11 '' .
I .
.

I
.
.

1 I1': ."I I
.
.

1
I
dens dislocation, namely, the alar ligaments and the trans­
I . . I
I II verse ligament of the axis.
I I I I
I I II I
I Huguenin (personal communication, 1980) points out
I
I
I : ; I : the clinical symptomatology and the potential changes
II I I
---
seen on radiographs as a result of either partial or complete
a c b c
tears involving the ligaments in the occipito-atlanto-axial
joint region, both in functional tomograms and CT scans.
Fig.3.19 Steel's rule of thirds (Steel, 1968):
a = b = 2c = 16(a + b + 2c)
a = dens axis
Biomechanics of the Lower Cervical
b spinal cord
Spine (0-C7)
=

c = safety zone

The axis represents a transitional vertebra between the


upper and lower cervical spine. The greatest range of mo­
tion takes place in the mid-cervical spine region with the
following possible motion directions: cervical flexion and
extension, side-bending (e. go, lateral bending or lateral
flexion), and rotation. The vertebral motion units (i. e.,
spinal segments) inferior to the axis represent the typical
cervical vertebrae, They have a similar joint and vertebral
body architecture, which aids in the load distribution. In
contradistinction to the thoracic and lumbar vertebrae, the
cervical vertebrae exhibit the uncinate processes laterally
(Fig. 3.20) (Luschka, 1858; T6nduri and Theiler, 1990).
The inclination of the mid- and lower cervical spine
facets is approximately 450 with respect to the horizontal
plane. The lower segments are sloped more steeply than
the upper segments (Fig. 3.21).
Panjabi et al. (1993) describe the three-dimensional

Fig. 3.20 Drawing of the uncovertebral jOints. (After Luschka, anatomy of the apophyseal joints (synonyms: zygapophy­
1858.) seal joints or facet joints). In the cervical spine, the vertebra
with the largest joint surface is the axis (C2:
200 mnl); the
next largest are C3 through C5 (101-107 mm2), and C6 and
C7 show the smallest joint surfaces (79 mm2). The facet
joint inclination, however, is smaller in the upper cervical
spinal joints than in those of the lower cervical spine. The
articular processes are located relatively laterally which
reduces motion due to the bony restrictions imposed by
the "transverse processes." The transverse processes,
flanked by the anterior and posterior tubercles, form the
sulcus for the spinal nerve. They also contain the transverse
foramina to allow passage of the vertebral artery.
The close proximity of the articular processes, sulcus,
/' and transverse foramina is of particular clinical relevance in
,/
x
the presence of a progressive spondyloarthropathy, for in­
stance, as the spinal nerve and vertebral artery may be
preferentially compressed (Fig. 3.22).
Fig.3.21 Facet joint inclinations and axes of motion for vertebra In the adolescent, the articular processes are covered by
C4. (After White and Panjabi, 1978.) a thin cartilage layer. The irregularities of the individual

54

Copyrighted Material
Biomechanics of the Lower Cervical Spine (0-C7)

articular processes are, in part, evened out by so called


meniscoids. Originally described by Penning and Tondury
(1964), the meniscoids are composed of fatty and connec­
tive tissue, which is richly vascularized and innervated
(Fig. 3.23).
The meniscoids appear to play a particularly important
role in the extension motion of the cervical spine. Ricken­
bacher et at. (1982) describe the meniscoids functioning as a
sort of "plastic filler material" for the otherwise dead space
and to compensate for the relatively thin cartilage layer.
It is not clear to what extent, if any, the mensicoids are
responsible for recurrences and exacerbations of neck pain
associated with segmental or somatic dysfunctions. Pen­
Fig.3.22 Axial section through the cervical spine at the level of the
ning and Tondury (1964) do not believe that the menis­
fourth cervical vertebra. One can see the intervertebral canals that
coids would be the cause of such painful situations. How­
allow transit of the vertebral artery. Also. this specimen clearly
ever, Rauschning (personal communication, 1995), on the demonstrates the very close spatial relationships between such
basis of his detailed anatomic preparations of the cervical important structures as the intervertebral joints, the spinal nerve,
spine, believes that such meniscoids may play a role to and the vertebral artery. (Courtesy of Prof. W. Rauschning.
Uppsala.)
some extent.
The anatomy of the cervical disk is similar to that in the
other regions of the spine as it contains an inner nucleus
pulposus that is surrounded by the outer annulus fibrosis.
The disk in the cervical spine is subject to lateral tears at
ages as early as 9 years and certainly within the first 20
years of life. In the adult, as a result of the repetitive
stresses introduced over time with each movement, the
tears may advance to become true joint spaces, namely.
the joints of Luschka (uncovertebral joints; Luschka. 1858)
(Fig.3.24).
Tondury and Theiler (1990) hypothesize that the disk
tears and joint formation are observed as early as child­
hood. and it is postulated that these changes may be a
result of the upright posture. They call this a transitional
period.
Lateral diskal tears may increase in size in the medial
Fig.3.23 Vascular supply and innervation in the cervical spine of a
direction to a point where the tears are large enough to
young man. This macrophotograph of the cranial-cervical region
form full-sized gaps ultimately spanning the entire diam­ was obtained with the head turned 90·. (Courtesy of Prof. S. Kubik.)
eter of the cervical intervertebral disk. Particularly in the
lower cervical spine. such gaps can progress to involve the
entire thickness of the disk. literally halving it. Such
changes have also been observed in otherwise healthy
adults as young as 20 and 30 years of age (Fig.3.2S).
Given these dramatic changes in the cervical disk as
early as the second and third decades of life. it would be
safe to assume that there is an ever-increasing instability in
the affected spinal segment or segments. Thus. stability in
the motion units then comes to rely progressively more on

Fig.3.24 Frontal section of the cervical spine of a 9-year-old child.


Remnants of the primary cartilage of the joint/synchondrosis are
visible. The arrow indicates the fissure formation in the lateral
portion of the intervertebral disk of C3-C4. (From T6ndury and
Theiler, 1990.)

Copyrighted Material 55
Blomechanical Principles of the Spine and Joints

Fig. 3.25 Frontal section through the cervical spine of a 33-year­ Fig.3.26 Frontal section through the intervertebral disk of a 24-
old man. Both intervertebral disks reveal transverse fissures. (From year-old man. One can see the ruptured disk with the laterally
Tiindury and Theiler, 1990.) displaced prolapsed nucleus pulposus, which is held back from
being extruded by only a few annular fibers. This conformation
then results in the compression of the associated spinal nerve (5).
(From Ttindury and Theiler, 1990.)

Fig.3.27 Hom-shaped progressive changes of the uncinate pro­


cesses between (4-(5 and (5-(5 (- ) .

a With anterior osteophyte formation.


b With posterior osteophyte formation.
R = Right
l = left

a .... ,)'- -..,f --;-';T --T' en" . •

the passive elements such as the longitudinal ligaments a sudden, acute disk herniation. At the same time, the
and the loose connective tissue, and even more so on the uncinate processes start to change their shape, assuming
active components, namely, the postural muscles. a "bull's horn" appearance, and the vertebral bodies appear
It is possible then that subsequent to a complete diskal to approximate each other. This can be seen in the standard
tear, the gelatinous material of the nucleus pulposus will be AP and lateral radiographs. The surface end-plates undergo
extruded dorsolaterally resulting in compression of the prominent sclerotic changes, which are best seen in the
associated spinal nerve. Clinically this can lead to classic lateral projection. There may sometimes be a small but
signs of disk herniation (Fig. 3.26). noticeable step-off or increased angulation above the area
Beginning around age 25 years, the nucleus pulposus of sclerosis, which is known as the Guentz sign (Fig. 3.27).
begins to desiccate, which in turn reduces the likelihood of

56

Copyrighted Material
Biomechanics of the Lower Cervical Spine (C3-C7)

Tondury and Theiler (1990) have demonstrated that


continued disk dehydration reduces the facet joint's ability
to adequately withstand the normal mechanical loading
forces, thus reducing its ability to adequately maintain
the position of the head.
With progressive dehydration, the uncovertebral struc­
tures assume a greater and greater role in bearing the
weight in the cervical spine. Again, these structural
changes can be seen in standard radiographs where the
uncovertebral joints demonstrate a bull-horn appearance.
With continued dehydration, the weight of the superior
vertebral body is increasingly borne by the uncinate pro­
cesses of its inferior joint partner. The uncinate processes
subsequently show signs of sclerosis and form a shallow
joint space in the form of a pseudoarthrosis. Ultimately the
uncinate processes become the major weight-bearing
structures. These structural changes bring the vertebral
artery and the individual spinal nerve into even closer
proximity.
The age-related "normal" changes described above must
be differentiated from those that result from trauma. Fig.3.28 Sagittal section through the zygapophyseal (facet) joints
at the lower cervical spine. The orientation of the articular process
Trauma to the cervical spine may actually tear the disk
is approximately 45°. (Courtesy of Prof. W. Rauschning, Uppsala.)
off the vertebral end-plate. A hematoma may then form
1 Meniscoid
between the disk and end-plate (Taylor and Twomey, 2 Spinal nerve
1993). 3 Ganglion

Facet Inclination and lVIovements

The inclination of the facets in the mid- and lower cervical


spine is approximately 45° with respect to the horizontal (1

plane. As one proceeds down the cervical spine, the facet


inclinations become progressively more steep, with the
upper ones being comparatively flat and the lower cervical
facets being more vertical (Figs. 3.21, 3.28).
The motions that are possible between the two vertebral
(4
partners in each spinal unit or vertebral segment are ac­
tually are a combination of translatory and rotatory move­
ments about the various axes in the three-dimensional
coordinate system.
For flexion and extension, Lysell (1969) describes a ra­
dius of curvature upon which the individual segments C7
move. The so-called segmental arch is nearly flat at (1
and almost semicircular at G, with that of (4 having an
intermediate configuration (Fig. 3.29). The top angle is a
function of the facet joint inclination angle and the shape of
the intervertebral disk.
Flexion-extension motion (±0X) is greatest in the mid­ Fig.3.29 The segmental arches. (After Lysell, 1969.)
cervical spine (Table 3.4 and Fig. 3.30). It is largest at the
(5-(6 segment where the flexion-extension motion mea­
sures approximately 17°. Arguably this may explain the Translatory motion in the cervical spine is a gliding
high incidence of cervical spondyloarthropathy in the motion in the sagittal plane (±) and amounts to approxi­
mid-cervical spine. mately 2.0-3.5 mm (White, 1975).

57
Copyrighted Material
Blomechanical Principles of the Spine and Joints

Table 3.4 Range of motion at the various cervical spinal levels. The average values were derived from Dvorak (1988d. e) and Penning
(1976. 1987a)

Spinal Segment Flexion/Extension Side- bending (Rotation)

--
Range
(degrees)
Vb WV
(2-(3 5-23 8 11-20

C3-(4 7-38 13 9-15 11 10-28 11

(4-(5 8-39 12 0-16 11 10-26 12

(5-(6 4-34 17 0-16 8 8-34 10

(6-C7 1-29 16 0-17 7 63-15 9

C7-T1 4-17 9 0-17 4 5-13 8

is accompanied simultaneously by rotation about the


y-axis and vice versa. Again. by convention. the point of
CO/C1
reference for describing vertebral motion between two
C1/C2 adjoining vertebrae is the anterior portion of the body of
the superior vertebra.
C2/C3
In the past. some authors have described motion by

C3/C4 inferring movement of the spinous processes. This is no


longer the standard international description. but for com­
C4/C5 pleteness it is included here. Assuming that side-bending
motion is being introduced to the cervical spine to the left.
C5/C6

E -
the associated convexity of the cervical spine is to the right.
C6/0 Thus. when describing motion of the spinous processes.
side-bending introduced to the left will be accompanied
C7/T1
by the spinous processes rotating to the right. that is.
o 10 20 30 40 50 toward the convexity. Again. description of vertebral mo­
tion using the spinous processes is no longer the standard.
II Rotation and it is recommended to utilize the current motion de­
• Side-bending scription conventions.
[] Flexion/extension
At the second cervical vertebra. there is 2° of coupled
axial rotation for every 3° of side-bending. At the seventh
Fig. 3.30 Schematic representation of the values of range of mo­ cervical vertebra. there is 1 ° of coupled rotation for every
tion (degrees) in the three major planes (rotation. side-bending.
7.5° of side-bending (Figs. 3.31, 3.32). The osteopathic liter­
flexion/extension). Values are those contained in Table 3.4. In the
ature describes this coupling of movements as type II or
upper cervical spine it is axial rotation that is the major motion
component. In the mid-cervical spine the major motion compo­ nonneutral type motion (Fryette. 1954; Ward and Sprafka.
nent is flexion and extension motion. 1981).
In clinical practice. the patient's active and passive range
of motion in the cervical spine can be assessed with the
Coupling Patterns: Side- bending assistance of a compass-like or gravity-activated gonio­
and Rotatory Motion meter. Alund and Larsson (1990) employed an electronic
goniometer for their measurements of three-dimensional
Lysell (1969) measured the coupling patterns for cervical range of motion. This improved the accuracy and reproduc­
side-bending and rotation. The coupling patterns are of ibility of spinal motion testing. in particular that of axial
significant clinical relevance and are routinely evaluated rotation. Since the measurements can easily be stored elec­
during the functional examination of the spine. tronically and retrieved quickly for comparison. this system
When the head undergoes side-bending toward one is useful for monitoring patients' progress.
side. there is simultaneous rotation in the cervical verte­ Berger (1990) presents another attempt to quantify the
brae toward the same side. Thus. rotation about the z-axis vertebral range of motion in the cervical spine. In this

58
Copyrighted Material
Biomechanics of the Lower Cervical Spine (O-G)

Left lateral bending I Neutral Right lateral bending


I I
I I

••••• I
I
I
I
••••
I
I
I
I
I

Fig.3.31 The major coupling patterns as related to the cervical spine. With permission from White and Panjabi, Clinical Biomechanics of
the Spine, Lippincott Williams & Wilkins, 1990.

proposed procedure, the patient is requested to move her


y
or his head while the examiner fixates one vertebra at a
time. The range of motion at a specific vertebral level is
then obtained simply by subtracting the various values
obtained between two adjoining vertebrae.
Utilizing the CA6000 Spine Motion Analyzer (Fig.3.33),
Dvorak et al. (1992 b) systematically examined the active
and passive range of motion of a group of nonsymptomatic
persons between the ages of 20 and 70 years. Based on the
Primary
data obtained from six well-placed precision potentiome­
L---v' movement
ters, the three-dimensional motion characteristics were
_ Coupled
stored electronically and analyzed using a computer. The
movement
various motion directions were analyzed according to age
and sex (Table 3.5, Fig.3.34). The following motion direc­
Fig.3.32 Coupled movements in the cervical spine: for example,
tions were specifically examined:
+0Z is accompanied by -0Y.

1. Flexion and extension (motion in the sagittal plane).


2. Side-bending (lateral bending). reliable and clinically relevant information, and serves as
3. Rotation in neutral position. a baseline for monitoring and follow-along of a patient's
4. Rotation with the spine maximally tlexed. course over time (Table 3.6).
5. Rotation with the spine maximally extended. In summary, our own studies demonstrate a significant
difference between a person's actively performed range of
As well as obtaining reliable, objectively reproduCible re­ motion and that induced or guided passively by the exam­
sults for cervical spine gross motion, this study also pro­ iner. The reproducibility of the passive range of motion
vided additional information about coupled motions. This turned out to be significantly better than that of active
computerized assessment may assist in obtaining more motion.

59
Copyrighted Material
BIomechanlcal Prlndples of the Spine and Joints

,.". '!. I
.-.
.

.f) �··b • 'It .h

Fig. 3.33 Measurement set- up for obtaining range-of-motion val­ d Side-bending left
ues with the assistance of the Spine Motion Analyzer. Note: the test e Rotation right
subject's trunk is held stationary. f Rotation left
a Flexion g Rotation with maximal flexion
b Extension h Rotation with maximal extension
c Side- bending right

Table 3.5 Normal range of motion values and standard deviations (in parenthesis) in the cervical spine, according to age and sex (Dvorak et
al., 1992b)

Age (Years)
20-29 30-39 40-49 50-59 60

FlexlonlExtenslon
- =
Men 152.7 (20.0) 141.1 (11.4) 131.1 (18.5) 136.3 (15.7) 116.3 (8.7)

Women 149.3 (11.7) 155.9 (23.1) 139.8 (13.0) 11 126.9 (14.8) 133.2 (7.6)

Side-bending
Men
--
101.3 (13.3) 94.7 (10.0) 83.7 (13.9) IJ 88.3 (29.1) 74.2 (14.3)

Women
--- -
100.0 (8.6)
"-
106.3 (18.1) 88.2 (16.1)
-= II 76.1 (10.2) 79.6 (18.0)

Axial rotation
- ---- =
Men 183.8 (11.8) 175.1 (9.9) 157.4 (19.5) 166.2 (14.1) 145.6 (13.1)

Women 182.4 (10.0) 186.0 (10.4) 168.2 (13.6) 151.9 (15.9) 154 (14.6)

Rotation with flexion


=
Men 75.5 (12.4) 66.0 (13.6) 71.5 (10.9) 77.7 (17.1) 79.4 (8.1)

Women 72.6 (12.7) 74.6 (10.5) 85.2 (14.8) 85.6 (9.9) 81.3 (21.2)

Rotation with extension


Men 161.8 (15.9) 158.4 (16.4) 146.2 (33.3) 145. 8 (21.2) 130.9 (24.1)

Women 11 171.5 (10.0) 165.8 (16.0) ..


153.9 (22.9) 132.4 (28.8) 154.5 (14.7)

60

Copyrighted Material
Vertebral Artery

Table 3.6 Examination findin gs of passive range of motion testing of the cervical spin e of a healthy adult

left Average Normal Percentage


(Flexion) Population of Normal

Flex i on/ extension 69 75 144 153 94%

Si de - bending 50 42 92 101 91%

Axial rotation 86 89 175 184 95%

Rotation from flexion 35 38 73 76 97%

Rotation from extension 84 80 164 162 101%

Fig. 3.34 Graphic representation of the various ranges of motion Fig.3.35 Course of the vertebral arteries.
measurements in a normal population between the ages 20 years
and older than 60 years. The representation is based on the data
presented in Table 3.6 (Dvorak et al.. 1992b.)

With the exception of rotation motion with the spine superiorly up to the level of the axis. After a slight postero­
nexed. the range of motion in all other directions decreases lateral curvature it leaves the costotransverse foramen of
progressively with advancing age. One explanation for the the atlas to continue in a posterosuperiorly directed loop
slight. albeit apparently paradoxical. increase in rotation that ultimately punctures the atlanto-occipital membrane
while the spine is held in the flexed position. and in and the dura mater in the region of the foramen magnum
particular at the atlantoaxial articulation. may be that this at the occiput (Fig.3.35).
area is least affected by degenerative or spondylotic Extreme rotation of the head can lead to neurological
changes. which allows for some compensation of the loss symptoms. such as dizziness. nausea, and tinnitus. These
of motion lower down in the mid-cervical and lower cer­ are often caused by a transiently decreased blood supply in
vical spine. the basilar region. since rotation of the head between 30°
and 45° to one side causes the blood flow to be diminished
in the opposite vertebral artery at the atlantoaxial junction
Vertebral Artery (Fig.3.36) (Fielding. 1957 ) .
Rotational instability in the upper cervical spine. in
The vertebral artery is an important structure in the cer­ either the congenital or acquired form (e. g.. by trauma).
vical spine. not only when approached from a structural­ may result in a mechanical reduction of the blood supply.
biomechanical aspect. but also when considering the Furthermore. due to the close anatomic proximity of the
various functional examination and treatment procedures vertebral artery with the margins of the (1 and (2 facet
employed in the field of manual medicine. The vertebral joints during rotation. mechanical irritation is possible.
artery enters the costotransverse foramina at the level of which can potentially lead to reflex spasms (Fig.3.37).
(6 on either side. occasionally that of (5. and extends Other factors such as spondylotic degenerative processes

61
Copyrighted Material
Biomechanical Prindples of the Spine and Joints

Fig.3.36a-c Course of the


vertebral artery as a result of
atlas rotation to the left (a)
and to the right (c); (b) neu­
tral position.

a b

a b

Fig.3.37
a Rotation of C1-C2 to the right.
b Rotation of C1-C2 to the left.
c Exposed vertebral artery on the left side with induced rotation
to the right.
1 Atlas
2 Axis
3 Dens of the axis
4 Articular process on the left
5 Vertebral artery
6 Posterior arch of the atlas

may also cause reflex spasms, especially in the advanced is any suspicion for potential complications, the routine
state (Fig. 3.38). examination procedures should be complemented by the
Figure 3.39 demonstrates the close spatial relationship appropriate provocation tests, and if necessary the patient
between the vertebral artery and the uncovertebral and should be referred for the appropriate diagnostic evalua­
zygapophyseal (facet) joints. tion of the vertebral artery.
Though extremely rare, it has been reported that the
"high-velocity, low-amplitude" thrust techniques can po­ Reclination or Cervical Extension Provocation Test
tentially lead to disastrous results (Dvorak and Orelli, With the patient sitting, the examiner carefully and slowly
1982). It is therefore recommended that whenever there introduces rotation to the head and cervical spine of the

62

Copyrighted Material
Vertebral Artery

patient (passive motion). both in the anatomic neutral artery, in particular in response to cervical spine motion.
position and with the neck extended. The patient is queried With an ultrasound probe approximately 15 em long in­
as to the presence or appearance of any symptoms associ­ serted into the oropharynx, the vertebral arteries can be
ated with the induced movements. visualized on either side at the (3-(4 level.

Kleijn Hanging Test


The patient is supine with the head beyond the examining
table supported by the examiner. From this "hanging" po­
sition, the head is passively rotated to both sides, While the
examiner observes the patient's eye movements (nystag­
mus). the patient is again asked to report any subjective
symptoms.

Ultrasound Examination
Noninvasive ultrasound examination of the carotid and
vertebral arteries can be helpful when one suspects verte­
bral basilar insufficiency. subclavian steal syndrome and a
hypersensitive carotid sinus syndrome, or risk factors for
cerebral vascular disease. The ultrasound examination pro­ Fig,3.38 Prominent degenerative change s affec ting the axis of a
vides additional objective information about the vertebral 64-year-old woman.

a b

c d

Fig.3.39 Representation of the vertebral artery at the level of the Intervertebral jOint
atlas and the mid-cervical spine. 2 Uncovertebral joint
a At the level of atlas. 3 Nerve root
b Axial cross-section in the mid-cervical spine. 4 Spinal ganglion
c Coronal section in the mid-cervical spine. 5 Vertebral artery
d Detailed view of the intervertebral canal.
(Courtesy of Prof. W. Rauschning. Uppsala.)

63
Copyrighted Material
8/omechonlcal Prindples of the Spine and Joints

The following four study parameters are diagnostically T7-T8 level, nexion and extension movement increases
relevant: progressively in the inferior direction.

1. The direction of blood flow. Side- bending (Lateral Bending)


2. Differences between the vertebral arteries (diastolic This motion occurs to essentially the same degree at all
phase and pulsation amplitude). thoracic spinal segments. There is very little intersegmen­
3. Response to carotid compression/massage. tal variation.
4. Changes noted upon induced rotation, flexion, and ex­

tension to the head and neck. Axial Rotation


Axial rotation in the thoracic spine is opposite to that
Since it is physiologically normal for blood flow to decrease encountered for the flexion and extension movement.
in response to normal cervical rotation, it is important to The segments from T1 through T7 and T8 can undergo
verify as soon as possible any abnormal blood flow changes, significantly greater rotational motion than their more in­
especially if there are findings of complete interruption of ferior counterparts (e.g., those segments below T7-T8).
flow (Adorjani, personal communication, 1980; Keller et aI.,
1976).

Biomechanics of the Thoracic Spine

The facets of the individual vertebrae show a twofold in­


clination, that is, inclination around the x-axis of 60° and
around the y-axis of 20° (Fig. 3.40). Nonetheless, these
doubly inclined facets allow rotation about all three axes:
that is, flexion and extension, side-bending, and axial ro­
x
/'
tation (Table 3.7). '-./

Flexion and Extension


Fig. 3.40 Facet joint inclination and axes of motion in a typical
The flexion/extension range of motion in the upper seg­
thoracic vertebra. With permission from White and Panjabi, Clinical
ments of the thoracic spine is rather limited. Starting at the Biomechanics of the Spine, Lippincott Williams & Wilkins, 1990.

Table 3.7 Range of motion at the various thoracic spinal levels. The average values were derived from White and Panjabi (1990)

Range Mean Range Mean


(degrees) (degrees) (degrees) (degrees)

T1-T2 3-5 4 5 5 14 14
- -- - _.- - -
T2-T3 3-5 4 5-7 6 4-12 8
---
- --
T3-T4 2-5 4 3-7 6 5-11 8
-- _._.. =-=:= - -- -
T4-T5 2-5 4 5-6 6 4-11 8
--- - -- _. -- --
T5-T6 3-5 4 5-6 6 5-11 8
-;- - - - " ._.

T6-T7 2-7 5 6 6 4-11 8

T7-T8 3-8 6 3-8 6 4-11 8


- - -.
T8-T9 3-8 6 4-7 6 6-7 7
- - ;..=--:- =- -_.- -
T9-T10 3-8 6 4-7 6 3-5 4
-- -
nO-T11 4-14 9 3-10 7 2-3 2

T11-T12 6-20 12 4-13 9 2-3 2

T12-L1 6-20 12 5-10 8 2-3 2

64

Copyrighted Material
Biomechanics of the Thorax and Ribs

y
Coupled Movements
According to Panjabi et al. (1978), coupled motion behavior
characteristics in the thoracic spine are similar to those
described for the cervical spine. Side-bending (lateral
bending, ±0Z) to one side is accompanied by axial rotation
to the same side (+0y) (Fig. 3.41).
Greenman (2003) and Mitchell and Mitchell (1979)
based on the work of Fryette (1954) distinguish two types
of coupled movements: Primary
Type J: (neutral motion characteristics): side-bending to movement

one side (± 0Z) is accompanied by axial rotation


Coupled
-
(± 0Y) to the opposite side. This can occur in both movement

the thoracic and lumbar spine as well as at the


craniocervical and lumbosacral junctions. Fig.3.41 Coupled movement in the thoracic spine. With -0Z, there
is +0Y.
Type II: (nonneutral motion characteristics): side-bending
to one side (± 0Z) is accompanied by axial rotation
(± 0Y) to the same side. It is noted here that,
according to the osteopathic literature, type II 2S tension - Side·bendlng - I
Axial Rotation

mechanics can occur in all regions of the spine, and 20

exclusively in the cervical spine. 15

10

According to the above criteria, and considering the normal


kyphotic curvature in the thoracic spine, side-bending in­ o
.
T1-
.
T2- 13- T4- T5 - ' T6- 17- T8-
'
T9- Tl0- T11- T12-
duced to the thoracic spine is typically accompanied by T2 13 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1

coupled type I movement.


Fig.3.42 Segmental range of motion measurements For the tho­
racic spine. The representation is based on the data presented in
Table 3.7.
Biomechanics of the Thorax and Ribs

It is well known that vertebral motion in the thoracic rigidity and stability of the longest portion of the vertebral
spine is small compared to that in the cervical and lumbar column. Strong ligaments further stabilize the costoverte­
spine. The range of motion between the individual velte­ bral and costotransverse joints (Fig. 3.43).
brae is limited due to the restrictive effect of the longi­ The relatively firm union between the sternum and the
tudinal ligament, the anulus fibrosus. and the spatial ar­ thoracic spine by way of the ribs markedly increases the
rangement of the spinous processes and the connections resistance of the spine against forces that cause rotation. An
to the ribs. interesting experiment was conducted by Schultz et al.
The ranges of motion for axial rotation, side-bending, (1974a,b): while loads were applied to individual ribs
and flexion/extension in the thoracic spine are graphically from different directions their mobility was measured. It
represented in Fig. 3.42. was noted that the second rib exhibited the greatest resis­
Kumar and Panjabi (1995) studied the motion character­ tance when the force was applied from the posteroanterior
istics of the thoracic spine of healthy adults. Measurements direction. The lowest stiffness or resistance (highest flexi­
were obtained with the subject having the eyes closed, bility) was exhibited by the tenth rib when loaded either
actively, passively and passive assisted. Active range of from the superior or from the inferior direction.
motion for the thoracic spine was approximately 60° to According to White and Panjabi (1990), the costoverte­
either side (48.8-88.5°); passive motion was increased by bral joints play a crucial role in the thoracic spine by
approximately 14°, with the greatest range possible in the maintaining the stability yet allowing sufficient segmental
more inferior thoracic segments. The authors discussed the mobility. Their function, in addition to the action of stabi­
role of muscle coordination during passive loading situa­ lizing the entire trunk, is verified in a mathematical model
tions and whether those muscular influences may influ­ by Andriacchi et al. (1974).
ence or prevent injury. Due to its connection to the stern um anteriorly through
The union of the thoracic spine with the ribs posteriorly the ribs, the thoracic spine is able to withstand relatively
and with the sternum anteriorly significantly increases the high loading forces when subjected to various physiologic

65
Copyrighted Material
Biomechanical Principles of the Spine and Joints

movements, in particular the extension component. The

..., , SpIllOU p!OCl!i.l COSt(t1111lBj


thorax as a whole also enhances axial mechanical stabiliza­

J.
IiTt1£.d.J.tf.la1 ·/!r14l.1
tion, particularly when subjected to anteroposterior com­
CosIOlfIlll1J\'t!fJ.: iIorllcuia �",IIIIU
1 1In1 ct , pression forces at the expense of mobility.

1 --
."
IOfCO tl:l1llfl
Cm.I IU Biomechanics of the Lumbar Spine
kDlr1:J
C.o- IOI:rlll'l.
...... HNdofr1b
fl.."". Motion in the lumbar spine is possible in all directions with
-,
flexion-extension being the primary direction and rotation
'C:WlmR!
being the least, with side-bending somewhere in the mid­
Vet'teb<.II1
""'" dle. These motion characteristics are easily be explained on
account of the inclination of the facet joints, which in the

Fig.3.43 Schematic representation of the costovertebral and the lumbar spine, "stand" vertically while facing forward at an
costotransverse joints. (From Schuenke, Thieme Atlas of Anatomy angle of 45° (Fig. 3.44). In general, and depending on the
Vol. I, 2007.) specific segmental level, lumbar flexion and extension mo­
1 Radial ligament of the head of the rib
tion in the sagittal plane (defined by motion about the x­
2 Costotransverse ligament
axis) is between 10° and 20°. Side-bending (coronal plane;
3 Ligament of the rib tubercle
4 Costotransverse articulation z-axis) is between 3° and 6°, with the smallest excursion
5 Articulation of the head of the rib being measured at the lumbosacral junction. The reverse is
true for axial rotation (about the y-axis), which shows
greatest excursion at the lumbosacral junction (Lumsden
and Morris, 1968) but otherwise measures only about 2°
y
throughout the remainder of the lumbar spine. The specific
values are listed in Table 3.8 and are graphically repre­

/
/
sented in Fig. 3.45.
/
/
<-
'"
...... / / Coupled Movements
.
Side-bending (±0Z) is strongly coupled to axial rotation
z (±0y) (Miles and Sullivan, 1961; White and Panjabi, 1990).
/
/
/ "/ In the lumbar spine, with its normal lordosis, side-bending
<- /
...... / x
to one side in the neutral position is accompanied by
-...../
rotation to the opposite side (Fig. 3.46).
The osteopathic literature (Mitchell et aI., 1995; Green­
Fig. 3.44 Facet inclination and axes of motion (degrees) of a typical
man, 2003) describes a more complex coupling of motion
lumbar vertebra. With permission from White and Panjabi, Clinical
depending on whether motion occurs with the spine in the
Biomechanics of the Spine, Lippincott Williams & Wilkins, 1990.
neutral or in the nonneutral position (that is, the spine is
either flexed or extended). When, for instance, the lumbar
spine is flexed (±0X) and side-bending is being introduced

30 toward one side (±0Z), there is coupled rotation (±0y) to the

25 same side as the induced side-bending (Fig. 3.47). Trans­

20 latory gliding in the sagittal plane (±y-axis) coupled to axial


• Axial Rotation
15 rotation, although very uncommon, has been reported to
• Side-bending
10 occur (Rolander, 1966).
o Flexion!
5 Extension

o
Objective Documentation of lumbar Range
L3- L4- L5- of Motion
L4 L5 Sl

Lumbar range of motion measurements, while routinely

Fig. 3.45 Average values for segmental ranges of motion in the used in the assessment of patients with a low back pain

lumbar spine. The representation is based on the data presented in syndrome, may vary considerably depending on the way
Table 3.8. they are obtained. According to the American Medical As­

66
Copyrighted Material
Biomechonics of the Lumbar Spine

Table 3.8 Range of motion at the various lumbar spinal levels. The average values were derived from Dvorak 1991 c, d.

Flexion/Extension Axial Rotation


(Rotation about x-axis) (Rotation about y-axis)

Range Mean Range Mean Range Mean


(degrees) (degrees) (degrees) (degrees) (degrees) (degrees)

9-16 12 3-8 6 1-3 2

11-18 14 3-9 6 1-3 2

l3-l4 12-18 15 5-10 8 1- 3 2

l4-l5 14-21 17 5-7 6 1-3 2

l5-S1 18-22 29 2-3 3 3-6 5

y y

-oy

Primary
Primary
movement
movement

Coupled Coupled
- - movement
movement

Fig.3.46 Coupled movement in the lumbar spine. +02 is accom­ Fig. 3.47 Coupled movement in the lumbar spine. With +0X, there
panied by +("y is +02 primary movement accompanied by -oy.

sociation guidelines (Cocchiarella and Andersson, 2001) There were no significant sex differences for flexion­
the measurements should be as objective as possible, es­ extension or for side-bending motion. There was also no
pecially when dealing with medicolegal or disability deter­ side-to-side difference noted at the various segmental
minations. levels for side-bending and rotation motion.
In clinical practice, the range of motion is determined by Not surprisingly, there is progressive motion loss with
use of various kinds of inclinometers, goniometers, and advancing age. The reduction of motion is statistically dif­
computer-generated data obtained with such machines as ferent from one decade to another (Fig. 3.49). Our own
the Isostation 8-200. In our own studies (Dvorak et aI., studies also revealed a progressive increase in lumbar
1995), we studied 104 healthy persons (52 men, 42 range of motion as the day progresses, with the greatest
women) ranging from 20 years to 70 years in age using increase noted in the morning hours (Dvorak et aI., 1995).
the CA5000 Spine Motion Analyzer. The lumbar range of The ranges of motion in the different directions accord­
motion was thus measured in all directions and according ing to various authors are listed in Tables 3.9-3.11.
to the three fundamental planes as described by the corre­ Passive range of motion for flexion-extension and rota­
sponding primary axis: flexion-extension in the sagittal tion movement is greater than that of active range of
plane with motion about the x-axis; side-bending in the motion. While passive motion testing provides more reli­
coronal plane with motion about the z-axis; axial rotation able numbers, active motion testing provides valuable in­
in the horizontal plane with rotation about the y-axis. formation about the coupled movements. An increase in
Similarly to the experimental set-up described for the cer­ movement was demonstrated after the examinees had
vical spine, six potentiometers were placed on the patient's performed stretching exercises (Dvorak et aI., 1995).
back (Fig. 3.48).

67
Copyrighted Material
Blomechanical Prlndples of the Spine and Joints

50_

Fig.3.48 Examination arrangement for measuring lumbar range of Fig. 3.49 Graphic representation demonstrating the age- related
motion in using the Spine Motion Analyzer (Dvorak et al., 1995). reduction in thoracolumbar flexion-extension and side-bending
motions. There appears to be a rather drastic reduction in the
flexion-extension motion after the second decade of life and a
prominent reduction in side- bending after the fourth decade.

Table 3.9 Range of motion at the different lumbar spinal levels according to various authors (flexion/extension)

Author
--- 12-L3 L3-L4 L4-LS LS-S1

1 8,2
-
Tanz In vivo
1953 14 5.6 7.6 8.6 12.2

Allbrook 1957 In vivo 20 6.0 8.0


-
13,0 19.0
-
I 18.0

Clayson et al. 1962 In vivo 26 12.6 : II 15.8


-
15.9
=

-
17.7
-
18.7

Froning and Frohmann 1968 In vivo 30 9.0


: II 11.0
- 13.0
-- 16.0
-. 17.0

- -
Pearcy et al. 1984 In vivo 13.0 14.0 13.0 16.0 14.0
= ._.

--
Hayes et al 1989 In vivo 59 7.0 9.0 10.0 13.0 14.0
=- =-
Dvorak and Panjabi 1991a. c In vivo 41 11.9
= II
-
14.5
::-
15.3
=
18.2
-
17.0

Yamamoto et al. 1989 In vitro 10 10.1 11 10,8 I 11.2 14.5 17.8

Table 3.10 Range of motion seen with side-bending (lateral flexion)

Name

Tanz

Pearcy et ai. 1984 In vivo 13.0 14.0 13.0 16.0 14.0

Dvorak and Panjabi 1981a.( In vivo 41 11.9 14.5 15.3 18.2 17.0

Yamamoto et ai. 1989 In vitro 10 10.1 10.8 11.2 14.5 17.8

Table 3.11 Range of motion seen with axial rotation

Name Year n L1-12 U-L3

Yamamoto et al. 1989 In v itr o 10 2.1 2.6

68
Copyrighted Material
Biomechanics of the Pelvic Girdle

Biomechanics of the Pelvic Girdle

The functional unit of the pelvic girdle comprises the sa­


crum. the ilium one either side. and the fifth lumbar ver­
tebra with their corresponding articulations at the sacroil­
iacjoints and the symphysis pubis. The sacroiliac joints are
representative of a diarthrosis but function as an am­
phiarthroses allowing some movement. albeit very mini­
mal. The sacroiliac joint takes on an auricular or a "C"
shape. with the convex side facing anteriorly and inferiorly
(Fig. 3.50). There is significant variation in size of the sa­
croiliac joint ranging from 5.3 cm to 8.0 cm in length and
1.8 cm to 4.1 cm in width (Schunke. 1938).

Microscopic Joint Anatomy Fig.3.50 Anatomic representation of the sacroiliac joint.

The sacroiliac joints are practically vertically oriented but


also have an oblique orientation with respect to the sagittal
plane. In an axial cut through the mid-portion of the sa- First decade. In children. the cartilage on the sacral side is
croiJiac joint. the posterior border of the sacrum is wider three to four times thicker than that on the iliac side. On the
posteriorly than anteriorly. The opposite relationships are iliac side. the bone and cartilage are interdigitated in a
seen in the inferior portion of the sacrum (Fig. 3.51). manner similar to that found in the cartilaginous growth
There are a number of significant differences between plates of the vertebrae or the symphysis pubis during the
the sacral and iliac surface of the sacroiliac joint. On the growth period. The joint capsule, even though already well
sacral side, the articular cartilage is about 2-3 mm thick, developed at this age, allows for great mobility of the joint,
whereas on the iliac side it is not thicker than 1.5 mm. In with gliding movement possible in any direction.
chemical composition, the sacral cartilage is primarily
made up of hyaline material, whereas the iliac cartilage Second decade. In the sacral cartilage of a 15-year-old, the
is comprised of fibrous material. Sacral cartilage contains divisions into cell-rich and cell-poor areas have become
large chondrocytes which are grouped in pairs and fill the even more pronounced, particularly in the deeper layers.
lacunae completely. These lacunae are distributed evenly The columnar appearance of the iliac cartilage remains
throughout the hyaline matrix of the cartilage. The unchanged. By the second decade, a cartilaginous joint
ground matrix on the sacral side is homogeneous, with space has developed behind the joint surface on each
little fibrous tissue present except in areas of degenera­ side. The joint space is perpendicular to the joint line. The
tion (Bowen and Cassidy. 1981). In contrast, the ground pronounced changes observed in the cartilage of this joint
matrix of the iliac cartilage is made up of thick bundles of space are more likely to be due to mechanical stress and
collagenous fibers. The lacunes, surrounded by colla­ potential damage to the growing cartilage than due to the
genous fibers. are filled with chondrocytes that tend to growth process itself (Putschar, 1931).
clump.
The function and thus the biomechanical behavior of Third decade. Growth-related changes cease to occur on
the sacroiliac joint are closely tied to the histologic the sacral side before they cease on the iliac side. It is not
changes that occur over time as a function of age. Early until the third decade that the iliac surface assumes a
anatomic studies have relied primarily on anatomical convex shape and the sacral side the corresponding con­
specimens obtained from older persons whose joints had cave shape. While the deeper layers appear to remain
likely undergone a certain degree of degeneration. Thus. histologically unchanged. the superficial joint surface starts
early reports of "normal" sacroiliac joint function may showing a number of crevices with rough edges and ero­
have inadvertently been based on faulty assumptions. sions, more so on the iliac side than on the sacral side
that is, by inferring the same function to be present in a (Bowen and Cassidy, 1981).
young healthy adult. It is therefore helpful to describe the
sacroiliac joint's function systematically according to dif­ Fourth decade. The capsule grows still thicker, accompa­
ferent age groups. nied by a proportional increase of the fibrous material in

69
Copyrighted Material
Biomechanical Principles of the Spine and Joints

being diminished in the presence of significant build-up


of chondrocytes. The ground matrix is infiltrated with fi­
brous material. Osteophytes at the sacroiliac joint have
been observed in 85% of men and 50% of women in the
fifth decade (Frigerio. 1974).

Sixth decade. Capsule and synovium continue to grow


thicker and stiffer. In particular. the iliac portion has lost
a a significant share of its cartilaginous substance to the
point of exposure of the subchondral bone. A thick layer
of flaky amorphous debris now covers both joint surfaces.
and the iliac surface can no longer be distinguished by its
blue appearance (Bowen and Cassidy. 1981). The sacral
portion is less affected. although superficial erosions and
fibrillation have been noted. Osteophytes. which are espe­
cially prominent on the superior and anterior margins of
the joint. continue to broaden and invade the joint space in
b
an interdigitating fashion. Thus. motion in the sacroiliac
joint is reduced significantly to a point where no motion
whatsoever is possible. Partial or complete ankylosis at this
age has been observed to occur in 60% of males. in contrast
to 15% of females (Frigerio.1974).

Seventh decade. Cartilage continues to undergo further


c atrophic changes on both sides. While the process may
have progressed to erosions and fibrill atory changes at
some locations. thus leading to only bone being present
Fig.3.51 Horizontal sections through the sacroiliac joints at vari­ at those portions of the articular surface. some of the
ous levels. cartilage may show material primarily devoid of living
a Superior level. cells. as well as signs of necrosis. The remainder of the
b Mid level.
cartilage reveals an increase in collagenous material and
c Inferior level.
clustering of chondrocytes. There is more amorphous ma­
terial in the joint space. and fibrous degenerative changes
the synovial layer. There is. however. a decrease in the have led to intra-articular fibrous interconnections. The
vasculature associated with the joint. The joint surface is joints may have undergone complete ankylosis in as
microscopically irregular and discontinuous. with flat­ many as 70% of the case (MacDonald and Hunt. 1952).
tened. longitudinal cells. At this age. the iliac cartilage Calcifications at the capsular attachments have also been
reveals clumping of chondrocytes into bundles. In contrast. observed on both joint surfaces.
and except for discrete rough edges at its margins. the
sacral hyaline cartilage appears unchanged. A number of Eighth decade. At this age. the joints have ankylosed in the
osteophytes may have developed at the margins. especially majority of cases. with significant calcification at the pe­
on the iliac side. The joint cavity contains flakelike clumps riphery of the fibrous capsule. Subcapsular osteophytes are
of yellow amorphous debris (Bowen and Cassidy. 1981). present in almost all of t he joints. and their interdigitation
Despite the apparent loss of elasticity at this age. overall is so pronounced that essentially any movement is prohib­
joint mobility continues to be good. ited. Diminished movement may be further compounded
by the presence of intra-articular fibrous connections (Bo­
Fifth decade. Degenerative processes continue to become wen and Cassidy. 1981). Erosions and necrotic changes.
increasingly prominent.with signs of irregular joint surface exposure of the deeper layers. and fibriJlatory changes
due to erosions. Eosinophils and amorphous clumps of are found to a significant degree in all joints. though less
exfoliated material have accumulated in the joint space. so on the sacral side. Subchondral bone has become thin
The iliac cartilage is more affected. with joint thickness and atrophied (Fig. 3.52).

70

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Biomechanics of the Pelvic Girdle

Ligaments Associated with the


Sacroiliac Joints

Of great importance. in addition to a taut joint capsule. are


the ligaments associated with the sacroiliac joint. There are
two major sets of ligaments. an anterior and a posterior
group. The anterior group is made up of the relatively weak
anterior sacroiliac ligament. whereas the posterior group
comprises stronger and thicker ligaments. the long and
short sacroiliac ligaments as well as the interosseous sa­
croiliac ligament.
The very thin and weak anterior sacroiliac ligament
represents the thickened portion of the joint capsule.
a
With sacroiliac joint motion it undergoes a laterally di­
rected stretch. The sensory innervation of the anterior
sacroiliac joint occurs via the anterior rami of the spinal
nerves of L2 and L3. The short and long sacroiliac ligaments
are sensorily supplied by the anterior rami of LS through S2
as well as the posterior rami of L1 through LS and Sl
througll S3. The interosseous ligament receives its sensory
supply from the dorsal rami of LS-S2.
According to Sutter (1977). the sacrum is suspended
from tile posterior prominence of the iliac tuberosity by
way of the interosseous sacroiliac ligament. The sacrum is
tightly secured by two factors: (1) by the safeguarding
function of the sacroiliac ligaments. which limit excess
motion; and (2) by the shape of the jOint itself and its
keystone-like arrangement wherein the sacrum is wedged b
between the two sides of the ilium. Forces that are directed
toward the sacrum and the innominate bones are coun­
tered by a "clamp down" mechanism due simply to the
anatomic arrangement of the joint with its inferior con­
vergence. This mechanism remains intact only as long as
the short sacroiliac ligaments allow the mechanically im­
portant posterior closure to occur between the sacrum and
the ilium on either side. If these ligaments are fail or
become weak. the affected iliac bone can deviate laterally
to a minor extent. When lateral movement of the iliac bone
occurs. the upper pole of the sacrum is obligatorily pulled
into a more posterior position. which in turn approximates
the prominence of the iliac tuberosity. This mechanism is
mediated by the short yet very strong interosseous sacroil­
iac ligament (Fig. 3.53).

Fig. 3.52 Age- related degenerative processes observed at the sa­


croiliac joint (Bowen and Cassidy. 1981).
a First decade.
b Fourth decade.
c Seventh decade.

71
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Biomechanlcal Prindples of the Spine and Joints

2. It has been extremely difficult in the past to design the


appropriate experiments, let alone to reach conclusive
interpretations of studies investigating the mechanics of
this joint.
2 2

3 Despite worldwide research effort and a number of


first-rate conferences devoted to this topic, a final, all­
encompassing description of the physiology of the
sacroiliac joint has not been presented thus far.
A brief review of the literature reveals that Hippocrates
and Vesalius believed that the sacroiliac joint is mobile. It is
interesting to note that Hippocrates had already surmised a
certain degree of mobility to occur at the sacroiliac joint
during pregnancy. In the 19th century, those in the field of
obstetrics and gynecology became particularly interested
a in the function and mechanics of the pelvic girdle. Some
authors report changes in measurement of the pelvic inlet
that could only be explained on the basis of apparent
motion in the sacroiliac joint.
A decrease in the diameter of the pelvic inlet was always
found to be associated with an increase in the pelvic outlet.
This led to the conclusion that the sacrum rotates around a
--...-'l-
. 2 horizontal axis. This rotational movement of the sacrum
has been termed nutation ("nodding") movement in the
literature. However, the anatomic location of this axis
·3 varies greatly according to the various authors.
Pitkin and Pheasant (1936) describe two types of rota­
b tion based on measuring the angle between a line that
connects the superior iliac spines and various lines con­
structed through the sacrum. In one type, the axis of rota­
Fig.3.53 Ligaments associated with the sacroiliac joint. (After tion is at the center of the sacroiliac joint at the tubercle
Kapandji 1974.) between the superior and inferior joint surface (Fig. 3.54,
a Superior view. the point labeled a).
b Medial view.
The second type is that in which the center of the axis is
Anterior sacroiliac ligament
located at the level of the symphysis pubis (Fig. 3.54, the
2 Interosseous sacroiliac ligament
3 Sacrum point labeled b). Duckworth (1970) refers to a nutation
4 Ilium movement with the axis of rotation being at the site of
the shortest and strongest portion of the interosseous lig­
ament (Fig. 3.54, the point labeled c). Beal (1982) reported
Function of the Sacroiliac Joint that the axis of rotation is at the inferior pole of the sa­
croiliac joint (Fig. 3.54, the point labeled d).
A detailed literature review of the sacroiliac joint in the As early as 1937, Lloyd pointed to the close relationship
medical aspect has been presented by Rudolf and Benecke between architectural shape and the stability of the sac­
(1985). roiliac joint. When the sacrum is more rectangular in shape,
Arguably the function and pathologic motions of the the associated sacroiliac joint has a rather vertical arrange-
sacroiliac joint have been the subject of more controversy ment, which is clinically more often associated with rela­
and more hypotheses than for any other joint in the human tively increased instability. This concept was developed
body. This may be primarily for two reasons: further by Delmas (1950) and confirmed by Sandoz (1981).
According to these and other functional considerations,
1. The role and significance of the sacroiliac joint and two main prototypes of sacroiliac jOint shapes have been
motion in the lumbopelvic mechanism are not as read­ described: (1) the so-called tight-profile shape; and (2) the
ily evident as those of the hip or knee joint, for instance. open-profile shape.

72

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Biomechanics of the Pelvic Girdle

• Tight-profile-shaped sacroiliac joint. Here, the joint


surfaces between the sacrum and ilium are practically

\
congruent, and the retroarticular space is relatively
small. The short and strong interosseous ligaments span
the entire narrow joint. In this type, the balance be­
tween mobility and stability is unquestionably shifted in
the direction of stability at the expense of mobility. This
configuration is more typical of the male pelvis
(Fig. 3.55).
• Open-profile-shaped sacroiliac joint. The joint surfa­
ces are less congruent, the retroarticular space being +b
wider and the interosseous ligaments longer than in the
tight-profile type. This configuration allows greater ---/
mobility while stability is, not surprisingly, reduced.
This type is found predominantly in women, often in Fig.3.54 Different positions for axis of rotation a llowing sacroiliac
association with an exaggerated lordosis (Fig. 3.56). nutation ("nodding") motion.

Again, with this type of joint shape there is a greater


preponderance of instability.

Either of these two archetypes occurs in approximately


25% of the population, with the remaining 50% being of
the mixed or intermediate type.
Weisl (1954), using controlled radiographic studies,
abandoned the conventional concept of a fixed axis to
describe sacral rotatory motion. Based on his carefully
performed geometric measurements, he concluded that
while the primary location of the axis of rotation is approx­
imately 10 cm below the promontory, it can undergo an
up-and-down movement of up to 5 cm. This description Fig.3.55 Sacrum: flat type.
implies that movement of the sacrum is not only rotatory
around one stationary axis but follows a translatory path as
well.
Kapandji (1974) and Colachis (1963) came to similar
conclusions. Both investigators confirmed that motion at
the sacroiliac joint is a combination of rotation and gliding
(e.g., translatory) movement. Sutter (1977) postulates four
axes of movement for the sacroiliac joint around which
movement can take place either unilaterally or bilaterally
(Fig.3.57).
Various other authors, applying modern diagnostic
techniques such as CT and three-dimensional modeling,
have shed some additional light on the three-dimensional Fig.3.56 Sacrum: wide type.
biodynamic mechanisms in the sacroiliac joint (Frigerio,
1974: Egund et al., 1978).
Even though these studies would fulfill the require­
ments of modern research, adequate clinical studies are than scientific "prooL" with many questions remaining
still lacking, especially with regard to sufficiently high unanswered.
patient numbers. Such investigations are needed to Lewit (1973) views the sacroiliac joint as an elastic
conclusively answer the question of sacroiliac joint move­ buffer zone between the spine and the lower limbs. Sandoz
ment, both qualitatively and quantitatively. Thus, the final (1981) suggests a similar concept. Rather than viewing the
answer regarding the physiology, the biomechanics, and joint purely in terms of translation (e. g.. gliding) and rota­
the clinical relevance of sacroi I iac joint movement remains tion, movement at the sacroiliac joint may more appropri­
a matter of interpretation, hypotheses, and projection more ately be viewed as that causing compression in a specific

73
Copyrighted Material
Biomechanical Principles of the Spine and Joints

a IL- _________________________________
__________________ L-__________________________________________ I b

Fig. 3.57 The various axes of motion for the sacroiliac joints. (After Sutter, 1977.)
a Anterior view.
b Posterior view.

be further separated into two unit-vector components, as


indicated by the two motion forces labeled F, and F2 in
Fig. 3.58. Fl is the force causing nutation (nodding, specific
motion of the sacrum), a movement controlled by the
sacrospinous and sacrotuberous ligaments, as well as a
portion of the superior sacroiliac ligaments (force Bl)'
Translatory displacement along the joint's longitudinal
F2 axis (F2 in Fig. 3.58) is counteracted by the inferior portion
of the sacroiliac ligaments (force B2, Fig. 3.58).
At the same time, the reactive ground force (R), trans­
mitted through the femur to the hip combines with the
body weight (G) to form a rotatory couple. This force causes
the iliac bone to tilt posteriorly (N2; also known as "coun­
ter-nutation"), which is a rotation in direction opposite to
that of sacral nutation (N" Fig. 3.59).
This interaction of the different forces applies to a per­
Fig.3.58 Loading force vectors associated with trunk weight and
son standing on one foot or to the stance phase during a
its unit vectors. (After Kapandji, 1974.)
person's gait cycle. The forces in that instance act upon the
C Body weight (gravity)
F, Nutation motion ipsilateral sacroiliac joint of the supporting or stance (non­
F2 Translatory force (displacement) swing) leg (Beal, 1982; Kapandji, 1974). The reaction of the
8, Pulling force exhibited by the superior interosseous ligament ground (R). transmitted by the supporting limb. elevates
82 Pulling force exhibited by the inferior interosseous ligament
the corresponding hip and bony pelvis. whereas the con­
tralateral hip tends to be pulled down by the weight of the
region while simultaneously producing distraction at an­ pelvis on the side of the unsupported leg.
other point or region along its path. The cushioning or The resultant forces thus described introduce a shearing
buffering function of the sacroiliac joint in erect posture type of pull at the symphysis pubis (Fig. 3.60). Tile descrip­
may therefore be best viewed within the context of the tion thus far takes into account passive (static) forces with­
sum of all forces that are directed toward the pelvic girdle out taking into account the important influence and actions
(Kapandji, 1974; Beal, 1982). of the various muscle groups (Kapandji. 1974).
The vertical vector of the gravitational force caused by Under physiologic conditions. the sacroiliac ligaments
the weight of the trunk is directed toward the superior exert such a strong force that they substantially limit gross
surface of the sacrum, that is, Sl (Fig. 3.58). As a result of movement. making objective measurements of particular
the anatomic arrangement of this joint, this vector (G) can motions extremely difficult. It should not be difficult. how­

74

Copyrighted Material
Biomechanics of the Pelvic Girdle

Fig. 3.59 Body posture and its effects on the sacroiliac joint. (After Fig.3.60 Shearing forces encountered at the symphysis pubis dur­
Kapandji, 1974.) ing one-legged stance phase. (After Kapandji, 1974.)
G Body weight (gravity) G Body weight (gravity)
R Reaction of the ground R Ground reaction
N, Nutation motion of sacrum 5,,52 Shearing forces
N2 Counter-nutation by the innominate bone

ever, to imagine how the various force vectors correspond­


ingly alternate and interplay during the walking cycle,
repetitively causing a temporary and physiologically "nor­
mal"-that is reversible-pelvic torsion (Lewit, 1968).
Grice (1980) points out that the general elastic give of
the pelvic articulations, together with the ilium's ability to
undergo respective flexion or extension movement (ac­
cording to the various motions during the gait cycle), re­
D
duces the torsional forces at the spine to a minimum during
walking.
The force interplay described above (forces G and R)
brings about alternating movement with each step at the
sacroiliac joint such that there is nutation movement at the
sacrum while the ilium is counter-nutated. The force dis­
tribution described applies to the stance leg.
a b
Additional forces are introduced with active muscle
action: during the early stance phase the major active
muscle groups are the gluteus maximus and the hamstring Fig.3.61 Early stance phase (a) and swing phase (b). (After Grice .

muscles (Fig. 3.61 a, labeled A and B, respectively). Due to 1980.)


the attachments of these muscles at the pelvis and lower A Gluteus maximus muscle
B Biceps femoris, semitendinosus, and semimembranosus
limb, the posterior superior iliac spine is pulled posteriorly,
muscles
a movement correlating with that described above as
C I liop soas muscle
"counter-nutation" (Fig. 3.61). D Qu a driceps femoris muscle
The other leg, now in swing phase, activates primarily
the iliopsoas muscle and quadriceps femoris muscle
(Fig. 3.61 b, labeled C and D, respectively). The forces motions including those at either sacroiliac joint. Move-
generated through this action cause the pelvis on the ment between the sacrum on one side and the ipsilateral
same side to rotate anteriorly (Fig. 3.61 b). During the gait ilium is such that the sacrum typically moves in a direction
cycle, there is then a rather dynamic and a predictably opposite to that of the ilium. Motion is more in an anterior
repetitive interplay between a number of relatively small and inferior direction on the stance side, and more poste­

75
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Blomechanlcal Principles of the Spine and Joints

Jacob and Kissling (1991 ,199 6) examined sacroiliac joint


motion clinically. USing a stereophotogrammeter, they de­
termined an average range of motion of1 .7° and translation
of 0.7 mm. This in-vivo study is in agreement with that of
Egund (1987).

Innervation of the Sacroiliac Joint

Except for the studies by 5010nen (1957), Fortin et al.


(1994a,b), and Grob et al. (1995), there are few, if any,
conclusive studies regarding the innervation of the sacroil­
iac joint.
5010nen (1957) reports that the innervation of the sa­
croiliac joint occurs via the anterior rami of the obturator
nerve. Grob et al. (1995) report that the sacroiliac joint is

Fig. 3.62 Innervation of the human sacroiliac joint and the asso­ exclusively innervated by the posterior primary rami of the
ciated ligaments. (From Kissling, 1997.) spinal nerves, 51 and 52. The posterior ligaments are in­
Left: The long posterior sacroiliac ligament is shown. nervated by the dorsal rami of 53 and 54. The dorsal rami of
Right: The superficial layer of the posterior sacroiliac ligame nt has
51 through 54 penetrate the sacroiliac ligaments, where
been r efle cted .

they give off fine branches to the gluteus maximus muscle


1 Medial cluneal nerves
2 Long posterior sacroiliac ligament and continue to the skin as the medial cluneal nerves
3 Sacrotuberous ligament (Fig. 3.62).
4 Sacrospinous ligament Grob et al. postulate that the painful irritation zones
associated with a symptomatic sacroiliac joint can be ex­
rior and superior on the swing side. This introduces a rota­ plained by the fact that the joint and the origin of the
tional component at the sacrum, which is transmitted to gluteus maximus muscle are innervated by the same dorsal
the lowest lumbar vertebra via the intervertebral disk. Due rami. In clinical practice, the irritation zones are diagnos­
to the counter-nutation of the ilium and the recruited tically ascertained through manual medicine approaches.
action of the iliolumbar ligament, this vertebra is actually Furthermore, Grob et al. believe that the diffuse buttock
rotated in the opposite direction (1IIi, 1951). pain may be explained either by direct irritation or by
Thus, it would be plausible to assume that rotation at pseudoradicular referred pain related to the spinal seg­
the lower lumbar spine during the gait cycle can be held to ments of 51 and 52.
a minimum as long as there is unrestricted motion at the
sacroiliac joint.
Dejung (1985 ) describes the sacroiliac syndrome or sa­ Biomechanical Principles and the Clinical
croiliac joint dysfunction in 58 patients predominately in Examination of the Sacroiliac Joint
the age range 2 0-40 years. In many cases, the patient
reported a history of low back pain, occasionally radiating One of the aims the manual medicine approach within the
to the buttock but rarely to the knee. The radiation of the neuromusculoskeletal examination process is to determine
pain is usually on the same side as the side of joint restric­ the presence of an anatomically identifiable structure or
tion. The symptoms are often related by the patient to lesion referable to the pelvic girdle that would explain the
either a previous fall onto the sacrum or concurrent preg­ patient's pain.
nancy. A similar description is given by Greenman (1986). The field of manual medicine has developed a number
Mobility at the lumbosacral junction is often remarkably of particular examination techniques for the sacroiliac
decreased. joint, which are routinely guided by the functional-struc­
Joint motion restriction due to a somatic dysfunction in tural approach. The functional-structural approach uses,
this area must be diagnostically differentiated from the loss among other examinations, the evaluation of the quality
of motion due to antalgic posture secondary to a herniated and quantity of possible range of motion, palpatory soft­
disk. In the latter case, the surrounding muscles may reveal tissue assessment, muscle evaluation for length and
localized muscle "spasm" or a hard palpable band, in par­ strength, and specific or provocation tests.
ticular in the gluteus maximus, longiSSimus lumborum,
adductor longus, iliopsoas, and piriformis muscles.

76

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Biomechanics of the Pelvic Girdle

The Functional-Structural Examination as Applied to tually moves superiorly when the patient flexes the thigh at
the Sacroiliac Joint the hip. During this test, in the "normal" unobstructed
1. Range of motion testing-quantity and quality of situation, hip flexion is associated with a "drop" of the
motion assessment. The goal with this examination PSIS on the side of the flexed hip.
step is to determine not only active and passive range of Bernard and Cassidy (1991) and Herzog et al. (1989)
motion but also the quality of movement, in particular examined the reliability of the flexion test and spine test
the end-feel. The examiner also observes which section in a symptomatic population. They found a high correlation
of the motion is painful along the arc of motion. While between the examination findings and their causative
the overall range of motion is relatively small, especially pathology.
when compared to any limb joint or even motion in the Dreyfuss et al. (1994) examined a group of nonsympto­
vertebral facet joints above, a detailed examination is matic adults in order to determine the incidence of false­
useful nonetheless as it may help localize the side of positive findings that might be encountered when using
dysfunction. the various sacroiliac screening tests. A large number of
2. Palpation of soft tissues. This examination component false-positive findings would reduce the specificity of a
assesses the soft tissues associated with and surround­ particular test.
ing the sacroiliacjoint as well as the irritation zones that At least one of the three tests (standing and seated
are correlated with the jOint. Specific provocation tests flexion tests, spine test) was found to be positive in 20% of
may be required to further delineate the patient's pain. the nonsymptomatic persons, and when analyzed accord­
3. Muscle testing for length and strength. The relevant ing to the sex distribution, positive findings were present in
key muscles and those associated with the sacroiliac 26% of the female participants and 12.5% in the male par­
joint are examined not only for their maximal strength ticipants. The authors concluded that, given the relatively
but also for any reduction in their normal length high level of false-positive findings, the presence of a pos­
(Dvorak and Dvorak, 1991). itive finding upon sacroiliac joint screening should be in­
4. Special tests and provocation tests. These routinely terpreted very carefully and clearly should not be viewed as
include the standing and seated flexion tests as well as the "sine qua non" finding for a sacroiliac joint dysfunction.
the spine test during the initial examination approach to As in other fields of medicine, it is useful to combine
pelvic girdle dysfunctions. multiple tests in order to arrive at a meaningful diagnosis.
As Griner et al. (1981) indicate, the specificity of the indi­
vidual test can be enhanced when a number of relevant
The Standing and Seated Flexion Tests tests are employed simultaneously rather than using a
The patient, either standing or sitting, is requested to ac­ single test in isolation.
tively flex and extend the thoracolumbar spine while the Leboeuf (1990) examined the sensitivity and specificity
examiner palpates the posterior superior iliac spine (PSIS) of seven lumbopelvic orthopedic tests in 20 nonsympto­
on either side and compares the presence or absence of any matic and 39 symptomatic persons but was unable to
movement of the posterior superior iliac spines with re­ predict the specific localization or dysfunction in the symp­
spect to each other. The test is denoted as positive when tomatic patients.
one PSIS moves more superiorly on one side in comparison Mior et a\. (1990) studied the inter-examiner reliability.
with the other side. The side on which PSIS motion is more While the intra-examiner reliability was very good, the
superior is denoted as the side of "positive" finding, as this inter-examiner reliability was unsatisfactory. The authors
is the side that is interpreted as the side of sacroiliac joint concluded that what appears to matter more than the
restriction of dysfunction. One of the potential explana­ individual practitioner's experience is the choice of the
tions for this is that the sacroiliac joint is "hung up" on appropriate combination of the relevant diagnostic tests.
that side-that is, motion is not free-and while bending McCombe et a\. (1989), examining the usefulness of pain
forward the ilium on the restricted side "pulls the PSIS" in a provocation tests, conclude that, with a determined kappa­
more superior direction as the pelvis rotates anteriorly. value of 0.16-0.63, the potential use of such tests can be
supported. Laslett and Wil.liams (1994) examined 51 pa­
The Spine Test tients using six different provocation tests including the
The spine test is performed with the patient standing while pelvic distraction and compression tests, pelvic torsion test
the examiner compares one PSIS with the center of the with left and right hip rotation, anterior sacral compression
sacroiliac joint. Taking the center of the sacroiliac joint as test, and a superiorly directed shearing test. Their findings
the point of reference, a positive test is one in which the indicate that the pelvic distraction and compression tests
PSIS does not move inferiorly, remains stationary, or ac- are quite reliable. as is the pelvic torsion test.

77
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Biomechonlcol Prindples of the Spine and JOints

In a study of 72 pregnant women, and using the poste­ the neutral zone observations and their relationship to
rior pelvic pain provocation test, Oestgaard et al. (1992) vertebral range of motion, Panjabi (1992a) has redefined
report sensitivity and specificity values of 81 % and 80%, the term clinical instability as follows:
respectively. While these figures appear to be rather high, it "Clinical instability is defined as a significant decrease in the
is noted that the provocation test was correlated with the capadty of the stabilizing system of the spine to maintain the
patient's subjective symptoms. intervertebral neutral zones within the physiologic limits so
that there is no neurologic dysfunction, no major deformity,
Adjunct Examinations of the Sacroiliac Joint and no incapacitating pain."
Radiographic studies and laboratory studies have but a Based on in-vitro and in-vivo studies, the basic hypoth­
very limited usefulness in the initial work-up of sacroiliac esis proposed by Panjabi is that the size of the neutral zone
joint-related pain and dysfunction (Davis and Lente, 1978; may serve as a better and more sensitive indicator of
Sturesson et aI., 1989). clinical spinal instability than does the overall range of
Sacroiliac joint injections, although technically demand­ motion.
ing, may reduce the patient's pain and thus serve both a The neutral zone increases significantly after trauma
diagnostic and a therapeutic purpose at the same time and fracture, while it is prominently decreased in situations
(Fortin et aI., 1994a, b). of increased muscular activity and internal spinal fixation.
In a high-speed trauma experiment using porcine cervical
Interim Summary spine specimens, both the neutral zone and range of mo­
Although it is currently not clear which specific test would tion were found to increase with the severity of injury
be the most appropriate for a particular patient or presen­ (Panjabi et aI., 1989a,b). However, the same study further
tation, it is safe to say that the use of multifunctional tests demonstrated that the increases in the neutral zone (mea­
can be expected to enhance the reliability of the entire sured as a percentage of the intact behavior) were signifi­
examination routine. When rationally chosen, and inte­ cantly larger than the corresponding increases in the range
grated within the entire clinical musculoskeletal diagnostic of motion for the same injury.
approach, manual medicine examination techniques for In another study from the same institute, spinal speci­
range of motion, soft-tissue assessment, and muscle eval­ mens were subjected to high-speed trauma of increasing
uation should all assist in delineating as specific a func­ severity. The investigators found the increase in f1exion­
tional and structural diagnosis otherwise not obtainable extension neutral zone to be the first indicator of the onset
through orthodox assessments. of injury (Panjabi and Oxland, 1993).
In an in-vitro experiment (Panjabi et aI., 1989a,b) and a
mathematical model of the spine (Nolte and Panjabi, 1989)
JOint Motion and Biomechanical the application of an anteriorly-inferiorly directed force
Correlations vector to the middle of the spinous process decreased the
neutral zone to the near intact value, while the range of
Clinical Instability-A New Hypothesis motion did not decrease. The important conclusions that
can be drawn from these two studies are summarized by
The graphic representation of the tissue behavior in the Panjabi (1992a) as follows:
different joints and vertebral motion segments reveals a "If there was an increased passive neutral zone-for example,
distinctly nonlinear shape. The response to imposed loads due to degeneration or trauma-then the muscles would be
and forces is rather complex owing to the intricate inter­ potentially capable of decreasing it and bringing it within the
play between a joint's architecture, friction, and the inher­ normal values. The same was not true for the range-of-mo­
ent tissue properties of the various soft-tissue components tion parameter."
including the tendons, ligaments, joint capsules, and Grob and Dvorak (1991) applied a small external fixator
muscles. In general, as described at the outset of this chap­ in order to stabilize a spinal motion segment temporarily in
ter, joint motion behavior can be broadly categorized into a the cervical spine. The fixator was used as a diagnostic tool
therapeutic and traumatic region (see Chapter 2, Fig. 2.5). to determine whether and to what extent its application
Panjabi (1992a) convincingly and elegantly presents a would diminish or even extinguish the patient's pain at a
new concept of spinal motion and instability. Previously particular segmental level. Once the pain-generating level
clinical instability has been defined as the loss of ability of had been successfully determined as the source of the pain,
the spine to maintain its pattern of displacement under the temporary application was exchanged for a permanent
physiologic loads so that there is no initial or additional one.
neurologic deficit, no major deformity, and no incapacitat­ To quantify the underlying motions responsible for the
ing pain (White and Panjabi, 1990). Within the context of pain, Panjabi et al. (1994) conducted an in-vitro study using

78

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Joint Motion and Biomechanical Correlations

fresh cadaveric human cervical spine specimens. The stabi­


lization was tested in the spinal segments of C4 through C6
(Fig. 3.63). Combining all of the results, the range of motion
Movable frame
decreased on average by only 38%, whereas the neutral
zone decreased by 71 % (Panajbi, 1992a).
The basic hypothesis originally presented by Panjabi
(1992a) proposes that the size of the neutral zone could
Cervical
represent a better, more useful indicator of clinical spinal
external
instability than does the overall range of motion. He also
argues that while the neutral zone in vivo has not been
measured directly, there is significant indirect evidence to
support the hypothesis.
In summary, on the basis of the above studies, the spinal Immovable frame
column exhibits nonlinear load-displacement behavior
(see Fig. 3.64), and the behavior is such that the spine is
highly flexible in the vicinity of the neutral posture. It is
hypothesized that in adverse conditions, the decrease in
neutral zone may be better correlated with the pain, and
that ultimately the reduction in the neutral zone is a better
indicator of instability than is the previously described
increase in gross spinal range of motion.
Motion within the neutral zone is rather free and unre­
stricted and involves minimum expenditure of muscular
energy (Panjabi, 1992a), whereas in the elastic zone, sig­
nificantly greater forces are required to induce motion.
As a descriptive demonstration, Figures 3.65 and 3.66
attempt to represent the above concepts graphically. A Fig. 3.63 An external fixator is applied to the cervical spine speci­
rather broad, almost flat container (e. g., a flat bowl) would mens. The light-sensitive markers are placed on the vertebral

be correlated with a relatively large neutral zone in a spinal bodies, where they register the three-dimensional intervertebral
motion via light sensors (Panjabi et aI., 1994).
segment, which would represent a rather unstable condi­
tion (Fig. 3.65a). A high-walled, steep container (e. g., wine
glass) would have a small neutral zone, indicating relatively
good spinal stability.
Force
As graphically represented in Figure 3.66, the neutral
zone in the "normal" situation is smaller than the pain­
ROM
free zone. When the spinal column becomes symptomatic, •
..

the neutral zone is increased beyond that of the pain-free


zone, which may be correlated with the patient's sensation
of pain, for instance.
The assumed increase in the neutral zone in the pres­
ence of clinical instability may be corrected by appropriate
fixation or ankylosing procedures, such as an external NZ
fixation or spinal fusion, or conversely, and if possible, .. •

through a coordinated muscle strengthening program,


which may then decrease the pathologically enlarged neu­ Range of motion

tral zone. This restoration of the normal neutral zone may


then reduce or extinguish the patient's pain. Fig. 3.64 The load-displacement curve demonstrating the non­
In application to a clinical presentation, Klein (2001) linear relationships between the range of motion (ROM) and force

examined patients with symptoms of whiplash-associated in a spinal segment. The entire range of motion can be subdivided
into a neutral zone (NZ) and an elastic zone (EZ).
disorder (WAD). He used EMG of the sternocleidomastoid
muscle and simultaneously used the C A-600 analyser to
measure the range of motion (ROM) of the cervical spine.
For the WAD patients it was impossible to reach even the

79
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Biomechanical Prindples of the Spine and Joints

Force

Force

ROM

NZ NZ

c==::: :--:---. b

Fig.3.65 Comparison model of instability versus stability. b A narrow drinking-glass-like structure is representative of a
a A flat bowl-like structure has a rather large neutral zone, corre­ relative stability with a small neutral zone.
sponding to relative instability. ROM Range of motion, NZ Neutral zone

Fig.3.66 Interpretation of the hypothesis of


mechanically induced pain as presented by
Range of motion (ROM)
Panajabi et al. (1994) .
• ..
Top: In the normal, nonpainful situation, the
D-,in_fr£:'le zone neutral zone is smaller than the pain­
free zone.
eutral Center: In the painful situation, as may be the

I I
zoni
Normal case in pain-induced with movement,

- . the neutral zone is larger than the pain­


free zone.
Bottom: In the pain-free situation, as may be
• .. accomplished with fixation, by use of

I
an external or internal fixator, or
through muscular activity, for instance,

Painful
.. -i==7 the neutral zone has been reduced
once again to fall below the level of a
pain-free zone.

. ..

Pain-free I.
I.1 )

elastic zone. They were "trapped" in the neutral zone, This hypothesis therefore represents the "next step,"
either unable or unwilling to move the cervical spine into wherein biomechanical factors are correlated with neuro-
a position that would seem to require additional muscle physiologic changes in order to look at a patient's pain not
activity, either due to the concomitant pain or to the fear of as an "isolated clinical fact" but rather as the expression of
precipitating it. their combination by the individual patient.

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4 Neurophysiology of the Joints and Muscles

Neuropathophysiology of the Articular Neurology


Apophyseal joints
The following presentation is based mainly on the funda­
The past 30 to 50 years have witnessed constantly increas­ mental work by Wyke and co-workers.
ing interest by physicians in manual medicine approaches. Articular neurology can be defined as that branch of
At the same tiine there has been an equal amount of neurology that deals with the morphology, physiology,
skepticism and overt criticism of the reported, primarily pathology, and clinical aspects of the innervation of the
empirical studies, since definitive basic and clinical re­ joints of the entire skeleton and the limbs. Within this
search was lacking. For a long time more hypothetical chapter, we will concentrate primarily, but not exclusively,
postulates than real science had been proposed in an at­ on the apophyseal joints, which are also referred to in the
tempt to explain the possible mechanisms of action that literature as the zygapophyseal ("Z-joints") or facet joints;
were thought to underlie the different manual medicine in this text the terms will be used interchangeably.
techniques. Despite recent notable progress and intensive Wyke's major contribution to the field of articular neu­
international efforts with better scientific designs and im­ rology was the identification of the structures and inner­
plementation of solid research protocols, little is still vation patterns of the four major joint receptor types, as
known today about the specific neurophysiologic processes well as their distribution and characteristic physiologic
or specific biochemical or biomechanical mechanisms that behavior. Furthermore, Wyke's work has shown that these
are initiated with or follow manipulation or mobilization reseptors can be found in all synovial joint capsules, and
maneuvers applied to the joints of the spine and the limbs. that they have an effect on static and dynamic reflex con­
One of the major initial steps was taken in 1975, when trol mechanisms of the skeletal muscles in response to
upon the recommendation of the National Institutes of normal and pathologic conditions.
Health, the National Institute of Neurological and Commu­
nicative Disorders and Stroke (Goldstein, 1975) held a con­
ference on the topic "The Research Status of Spinal Manip­ Receptors of the Joint Capsule
ulative Therapy." References here are mainly to Sato's
(1975) work on the somatosympathetic reflexes, Perl's It is now accepted that the human synovial joints contain
(1975) work on pain and spinal and peripheral nerve fac­ three types of mechanoreceptors (nociceptive-free) and
tors, and White and Panjabi's (1990) fundamental work on the free nerve endings-the nociceptors. Their organization
the biomechanics of the spine. was visualized in neurohistologic studies (Wyke and Pola­
In 1978, a symposium was held in Pisa, Italy on "Reflex cek, 1973, 1975; Freeman and Wyke, 1967; Vrettos and
Control of Posture and Movement" (Granit and Pompeiano, Wyke, 1979).
1979). Even though manual medicine per se was not dis­ The mechanoreceptors are proprioceptors and can be
cussed, this symposium offered a broad basis of the theo­ further subdivided into three specific groups (types I. II. and
retical research in this field up until that time. III), while the nociceptors make up the fourth group (type
In 1982, the College of Osteopathic Medicine at Michi­ IV). They are depicted in Figures 4.1 and 4.2 and are de­
gan State University held a symposium entitled "Empirical scribed in more detail below.
Approaches to the Validation of Manual Medicine" (Green­
man and Buerger, 1984). Here, researchers and clinicians Type I Receptors (Mechanoreceptors)
from the fields of biomechanics and neurophysiology dis­ The type I mechanoreceptors are found primarily in the
cussed their basic and clinical research findings in relation outer layers of the fibrous joint capsule. These receptors
to the field of manual medicine. consist of three to eight globular corpuscles measuring
Based on his basic experimental research with Freeman approximately 100 i-lm by 40 pm. Thinly encapsulated and
(Freeman and Wyke, 1967), Wyke coined the term "articu­ thinly myelinated afferent nerve fibers (6-9 i-lm) connect
lar neurology." Wyke's publications from 1967, 1975 (to­ these corpuscles with the corresponding articular branches
gether with Polacek), 1979, and 1980, and the information of the dorsal rami of the spinal nerves.
presented by Jayson (1980) expand on this term and thus
provide a basis for a better understanding of the neuro­
physiologic processes that are potentially involved in man­
ual medicine. These will now be described in more detail.

81

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Neurophysiology of the Joints and Muscles

#' r,;;:J-
., f' J'­
,
, '
/,­
h: -:- '
\---::; .../';/

Type II Type I I I Type IV

Fig.4.1 Schematic representation of the four joint receptors. The type I, II, and III receptors are mechanoreceptors. Type IV receptors are
nociceptors (Polacek, 1966).

Function
• Rapidly adapting mechanoreceptors with a low thresh­
old reacting to changes in tension of the fibrous joint
capsule (less than 0.5 seconds).
• Phasic and reflexogenic effects on neck, limb, jaw, and
Type I
eye muscles.
• Transitory inhibition of the nociceptive activity of the
Type II
joint capsule.

Type III
Type III Receptors (Mechanoreceptors)
Mechanoreceptors of the type III category play a significant
role in joint function. The type III receptors are typically
embedded in the ligaments and the terminal portion of the·
tendons close to the joint capsule. They are not found in the
joint capsule itself. Morphologically, they consist of broad,
Fig.4.2 Location of the various joint receptor types demonstrated
fusiform corpuscles (600 11m by 100 11m) and usually ap­
for the knee joint. (After Freeman and Wyke, 1967.)
pear singly. Occasionally, they occur in clusters of one to
three and are found at the end of a ligament or tendon.
Function The type III receptors are innervated by large myelin­
• Slowly adapting receptors: they control tension of the ated (13-17 11m) fibers that are connected to the articular
outer layers of the joint capsule. branches. The shape of the type III receptors resembles that
• Transsynaptic inhibition of the centripetal flow of the of the Golgi tendon organs. It is postulated that the type III
activity of the nociceptive afferent receptors (type IV mechanoreceptors may have a function similar to that of
nociceptors); in other words, inhibition of the impulses the Golgi tendon organs. Furthermore, it is believed that
arising from pain receptors. these slowly adapting receptors have an inhibitory reflexo­
• Tonic reflexogenic effects on the motor neurons of the genic effect on motor neurons (Freeman and Wyke, 1967).
necl<, limb, jaw, and eye muscles (Wyke 1975, 1977;
Molina et aI., 1976; Biemond and Dejong, 1969; Igarashi Function
et aI., 1972; Hikosaka and Maeda, 1973; Dejong et aI., • Inhibitory reflexogenic effects on motor neurons.
1977). • Function similar to the Golgi tendon organ.

Type II Receptors (Mechanoreceptors) Type IV Receptors (Nociceptors)


The type 1\ receptors consist of oblong, conical, thickly Nociceptive fibers are sensitive to noxious substances in
encapsulated corpuscles (about 280 11m by 100 11m) that the tissue. Nociceptors are free, very thinly myelinated or
most often appear singly in the deeper layers of the fibrous nonmyelinated plexiform nerve endings. They are ubiqui­
joint capsule. These receptors are connected to the articular tous in the fibrous portion of the joint capsule. This recep­
rami by way of thickly myelinated nerve fibers. tor system is activated by depolarization of the nerve fibers.
For instance, depolarization occurs with constant pressure
on the joint capsule as would be the case with nonphysio­

82

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Articular Neurology

logical position or as is seen with abrupt, jerky, uncon­ Innervation of the Joint Capsule
trolled movement. They are set off by such tissue altera­
tions as disk narrowing or compression, acute vertebral The joint is innervated by the dorsal rami of the associated
fracture, or a dislocation of the apophyseal joints, In addi­ spinal nerves. It should be emphasized that the articular
tion to mechanical factors, the nociceptors can also be ramus of a nerve root contributes not only to one segmen­
stimulated by chemical irritation via such substances as tal joint capsule: its collateral rami above and below also
potassium ions, lactic acid, 5-hydroxytryptamine, and his­ supply the neighboring joints as well. Therefore, the joint
tamine, among others. Interstitia.1 edema of the joint cap­ capsules are innervated bisegmentally or even multiseg­
sule, often associated with acute or chronic inflammatory mentally (Auteroche, 1983).
processes, is also known to activate the fibers, resulting in The cross-sectional representation at the level of the
pain. thoracic spine is depicted in FigA.3. This depiction dem­
onstrates the course of the nerve as it supplies the corre­
Function sponding joints, tendons, paravertebral muscles, and the
• Pain generation. periosteum.
• Tonic reflexogenic effects on neck, limb, jaw, and eye
muscles.
• Respiratory and cardiovascular reflexogenic effects.

6.

a L-__________________________________________ ______________________________________ b

Fig. 4.3a, b The nerve supply of the joints, muscles, ligaments, and Apophyseal joint
periosteum in the thoracic spine region. (After Wyke, 1967.) 2 Costovertebral joint
a Innervation of the vertebrae and disks, lateral view. Note that 3 Costotransverse joint
typically each facet joint receives its innervation of at least two 4 Spinal ganglion
neighboring branches. 5 Anterior ramus of the spinal nerve (left)
b Cross-sectional schema of the localized vertebral, disk and facet 6 Posterior ramus of the spinal nerve (left)
joint innervation as demonstrated in a thoracic vertebra. Note 7 Anterior longitudinal ligament
that typically the posterior primary ramus innervates the para­ 8 Posterior longitudinal ligament
vertebral muscles of the back, whereas the anterior primary 9 Paravertebral muscles
ramus innervates the extremities. Note the relationship of the 10 Interspinous ligament
spinal ganglion with reference to the facet joint posteriorly and 11 Ventral nerve root of the spinal nerve
the costovertebral joint anterolaterally. 12 Dorsal nerve root of the spinal nerve

Fig.4.3c C>

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Neurophysiology of the Joints and Muscles

Fig.4.3c Innervation of the


disk with emphasis on the

Anterior sinuvertebral nerve (Halde­


Nucleus pulposus ------ . �------

longitudinal mann et aI., 2002).


Sympathetic ganglion -----..
ligament
Gay ramus------
communicans
Sinu-vertebral nerve .,v-.A Annulus fibrosis
Spinal nerve
Anterior primary division
Posterior primary division-
-- 7
.?!
: .
Posterior
longitudinal

_I
ligament

Dorsal root ganglion --


Dura mater

other sensory modalities, such as that of light touch, re­


Central Interactions of the Mechanoreceptors mains intact, however (Yoshimura and North, 1983).
and Nociceptive Impulses It is possible that opioids inhibit those cells of the sub­
stantia gelatinosa that function as interneurons in the
The nociceptive and mechanoreceptive fibers enter the transmission of pain. Electron-microscopic studies showed
posterior horn in the gray matter of the spinal cord via an endogenous en kephalin in the substantia gelatinosa
the dorsal root. Once in the spinal cord, the nociceptive (Benett et ai., 1982), which again would support the idea
fibers divide into a number of collateral rami. of the interneurons performing an inhibitory function. The
Some of these rami extend through the gray matter di­ enkephalins have been surmised to function as inhibiting
rectly to the basal nuclei (basal spinal nucleus or laminae IV neurotransmi tters.
and V after Rexed). From there, they run through the lateral It also appears that strong stimulation of the type II
spinothalamic tract (anterolateral portion) to ultimately ter­ mechanoreceptors can lead to a depotlike increase of the
minate in the limbic system, where the actual perception of enkephalins in the dorsal horns (Wyke, personal commu­
pain occurs. Pain cannot be subjectively perceived unless nication, 1983).
depolarization of the synapse has occurred at the level of
the basal nuclei following the initial nociceptive impulses.
Similarly to the nociceptive afferent fibers, the mecha­ Mechanoreceptors and I\lociceptive Reflexes
noreceptive afferent fibers enter the posterior horn of the
gray matter of the spinal cord through the dorsal root As outlined earlier in this chapter, one of the major con­
(Fig. 4.4). tributions to the current understanding and the basis for
It is important for this theory that some of the many further research of the clinically observed nonradicular
divided rami form synapses at the level of the apical spinal pain syndromes, and the spondylogenic reflex syndrome
nucleus or lamina II (after Rexed). The apical spinal inter­ (SRS: see Chapter 6) in particular, came from Wyke and his
neurons arising from this level conduct the activity of the co-workers. This experimental work is of particular rele­
mechanoreceptive afferent stimuli to the basal spinal nu­ vance for clinical practice and for our current understand­
cleus, where they are thought to inhibit presynaptically the ing of the various proposed mechanisms.
pain-inducing nociceptive neurons. Thus, they interrupt The joint capsule and the articular nerve of C3-C4 were
conduction to the spinothalamic tract and the limbic sys­ microsurgically exposed in anesthetized cats. The joint
tem (Wyke, 1979a,b; Bonica and Albe-Fessard, 1980). capsule was irritated using a probe and a stimulator. A
Experiments on adult cats demonstrate that a portion of substantially lower voltage was necessal)' to stimulate
the thinly myelinated afferent fibers end in the substantia the mechanoreceptors (2 V) than to stimulate the nocicep­
gelatinosa of the dorsal horns. The transmission of noci­ tors ( 8 V). Wyke's results, as reproduced here, very clearly
ceptive impulses-as initiated by peripheral stimulation of show the reflex relationships between the receptors of the
the nociceptors, for instance-can be blocked by applica­ fibrous joint capsule, the apophyseal (facet) joints, and the
tion of opioids to the substantia gelatinosa. Transmission of peripheral musculature (Figs. 4.5-4.8).

84

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Articular Neurology

Afferent fi ber s Affe re nt f ib er s from mec ha no rece pto rs


from nociceptors (Ap-fibers) Lim bi c s y st em
(AO. (-fibers)

t
h l i
Spi not a am c t r a ct

Neurons In dorsal hom


Inhibiting intemeuron
Basal nucleus
t
Dorsal root

Anterior
spinothalamic
t
Nociceptors
tract

Fig.4.4 Arrangement of the fibers of the mechanoreceptors and nociceptors in dorsal horn of the spinal cord. (After Wyke. 1979 a.)

Left sea lene


]
Right scalene
]
Left sternocleidomastoid "J4� 11.... .....It••'"''''1'1 ....,.... I nW'." •. Wit..... ]
Right sternocleidomastoid ..ruu"..'t......* t tt_.I••tll'l.t!... ]
Left trapezius
�4��.�'���ii�il.f.fIIoWA� ]
Right trapezius
......... "1 ·" ]
Left digastric
]
Right digastric 'r" « "!rI S +,! ".,
I ,""-<
I ""
. • ' { f. r1'''
'' ''' ' "'.'f4I41 ""· fofIr'-"'.""."'''' ''''
''",'''
''''''''''.''•••'''''' l
.J

.....
2 VIS Hz/S ms

Fig.4.5 The reflexogenic mechanoreceptor effects of a cervical apophyseal joint on the muscles of the neck. At the location indicated by
the arrow. a single articular nerve of the left (3-(4 apophyseal joint was stimulated for 3 seconds with an electrical impulse (2 V. S Hz.
S ms) that selectively excited the mechanoreceptive afferent fibers in the exposed nerve. The simultaneous electromyographic tracings
show a long-lasting effect on the homologous pairs of the neck muscles. (After Wyke. 1979a.)

Akio Sato (1975) made similar observations in his inves­


tigation of the somatosympathetic refiexes. A refiex type of Possible Neural Mechanisms Involved in Back
relationship between soft-tissue changes or segmental Pain
(i.e., somatic) dysfunctions and diseases of internal organs
has been suggested on the basis of clinical observations The free nerve endings associated with the nociceptors are
(Beal. 1984; Beal and Dvorak. 1984; Larson, 1976). Perl found in the joint capsules, muscles (Mense and Meyer.
(1975) partially explains the phenomenon of referred 1985), the intervertebral disks (Bodgduk, 1993), and the
pain by this refiex mechanism. Wyke (1979b) suspects dorsal nerve root ganglia. They are all sensitive to pressure.
that multisynaptic intraspinal tracts may be involved. A sensory volley up to 25 minutes after compression of
which both ascend to the brainstem and descend to the the ganglion was detected. The ganglion may be a signifi­
basal nuclei of the lower levels of the spinal cord. cant source of a patient's pain. especially when considering

85

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Neurophysiology of the Joints and Musdes

Left scalene 1"".1.''''4� ,•• I..... 1:1,......... i4...., ._,.....


Left sternocleidomastoid .. �4 I ., •• 11.'""11,'.,_1

Left trapezius ]

Left digastric

Right scalene .,..... . ,'" ... • J


Rightstemocleidomastoid .... n. If. F It. "..,..w..,On1••'JQII. f,.P"".04I•• ]
Right trapezius 'I , ,.'. &1>'" PI' 't • _It p" . .... t • T."" ]

'--,.,. 5
Right digastric
]
.. 100 V
8 VIS Hz/S ms

Fig.4.6 The same experimental arrangement as in Fig. 4.5, except with a stimulus of 8 volts, 5 hertz, 5 milliseconds, in which both the
afferent fibers of the mechanoreceptors and nociceptors were stimulated. (After Wyke 1979a.)

Left biceps brachii


Left triceps brachii
Left rectus femoris -----
...
...... .1 ]
Left biceps brachii

Left triceps brachii


""'
_�i\� t .I•• ] ll
Left biceps femoris
---.ollll'
rill
__•• ' ] Left rectus femoris
""'404••I':_,(I1'I$ J
Left biceps femoris •
'''b *It 4 ]
Right biceps brachii 'W .It • lit......ti•• ]
Right triceps brachii "MIa' Is' .. .I "c... J
2s Right rectus femoris
,U ' J.. . "'''''
_ , . ..' ' .' J
Right biceps femoris '.'_Plat'••• I.I.". t d J
Fig.4.7 Reflex effects of the mechanoreceptors of the cervical .
50 v
apophyseal joints on limb muscles. At the signal (5), a single, '---'--.J

exposed branch of the articular nerve was repetitively stimulated 2s

for 3 seconds, selectively exciting the mechanoreceptor afferent


fibers in the corresponding nerve. The simultaneous electromyo­ Fig.4.8 The reflex effects of an induced manipulative procedure
graphic tracings of the upper and lower limb muscles display the directed at the (3-(4 articulation. At the signal, brisk vertical
reflexogenic effects of varying duration. They demonstrate that cervical traction procedure was applied to the isolated jOint. The
such stimulation has an affect not only on the muscles of the neck simultaneous electromyographic traCings of the homologous pairs
but also on the muscles of the extremities. (see also Fig.4.5). of the upper and lower limb muscles display the reflex effects of
Interestingly, stimulation that generates a nociceptive impulse such cervical manipulation on the peripheral musculature. (After
produces a different muscle potential response. (After Wyke Wyke, 1979a.)
1979a.)

its close proximity to the disk and in particular when there It has been postulated that the nucleus pulposus may
is a significant disk herniation (e. g., prolapse, protrusion). contain chemical substances that, when released from the
The dorsal nerve root itself does not appear to be partic­ disk after a tear, for instance, may induce inflammatory
ularly pressure sensitive unless there is concomitant in­ neurodegenerative reactions. Furthermore, it was thought
flammation or irritation. In a rabbit model, sensory dis­ that in the acute phase these chemical irritants are excita­
charge lasting up to several minutes after induced com­ tory rather than inhibitory.
pression of the nerve root by the autologous nucleus Olmarker and Rydevik (1993) believe that the immuno­
pulposus was observed. globulin G or stromolysin may be one of the chemical

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irritants. These observations may. at least in part, explain


Human Skeletal Muscle Fiber Types
the unabated pain reported by a significant number of
patients, even when decompressive spinal surgery had Muscle fibers are categorized according to their biochem­
been deemed successful after nerve root compression, for ical, histochemical, mechanical, and metabolic character­
instance. istics (Barnard et aI., 1971; Dubowitz, 1985; Cumming et
al" 1994). Until quite recently, striated muscles had simply
been classified according to their primary metabolic ac­
tivity as either aerobic or anaerobic muscle, or red and
Functional Pathology of Muscle white muscle, respectively. Recent research, however, in­
dicated that further subclassifications was necessary, es­
Morphology and Function of the Slow-Twitch pecially for the "white" fibers, which are more accurately
(Type I) and Fast-Twitch Muscle Fibers (Type II) known as "type 1/" fibers. While the literature had re­
ported "intermediate" muscle fibers that appear to share
Human skeletal muscle is characterized by a high degree of properties of both the aerobic and anaerobic fiber types,
plasticity. This plasticity is accomplished by a wide array of specific staining techniques have allowed separation of
different muscle fiber types, which allows the various the various fibers according to their particular metabolic
muscles to respond to the many different functional re­ and contractile properties. Despite the advent of more
quirements placed upon them (Pene, 1990). This explains, detailed histochemical profiles, this has also led to a con­
at least in part, the muscles' abilities to respond to different fusing nomenclature for the different types of muscle
demands. On the one hand, a person is abl.e to perform fibers (Cumming et aI., 1994). The salient characteristics
high-speed activities of short duration such as a hundred­ are listed in Table 4.1.
meter dash, while on the other the same person is able to The primary categorization distinguishes between the
run at slower speeds over long duration as is required in a slow-twitch, oxidative, fatigue-resistant type I fibers, and
marathon. The ability to develop sufficient strength for the fast-twitch, glycolytic type" fibers, which are further
activities such as lifting a 200-kilogram weight is yet an­ subdivided according to their fatigability. The type IIA fi­
other aspect of the muscles' functional plasticities to re­ bers are the fast-twitch, fatigue-resistant, glycolytic fibers,
spond to different demands. while the type liB fibers are also fast-twitch and glycolytic
Fluck and Hoppeler (2003 ) present a state-of-the-art but fast-fatiguing fibers.
review of muscle structure and function in which they Recent studies seem to indicate that human type liB
describe a muscle's plasticity in response to various stimuli fibers may correspond to the II-x fibers described for ani­
as well as developing a paradigm for studying gene regu­ mals (Ennion et aI., 1994; Smerdu et aI., 1994), and the
latory phenomena in humans. nomenclature has recently changed accordingly.
The following section on muscle fibers is based on the
excellent review presented by Weber (1995), which is re­
produced here with kind permission.

Table 4.1 Histochemical, biochemical, and phys i o l ogi c classifications of the three major muscle fiber types (after Barnard et aI., 1971;
Cumming et aI., 1994, Dubowitz, 1985)

H istochemica l Bioch emica l!


Classification Physiologic Classification

Brooke, Kaiser (1970) Barnard et al. (1971) Peter et al. (1972)

Slow-twitch SO S
Red Slow twitch oxidative
- Slow twitch
-

Fatigue-resistant

IIA Fast-twitch intermediate FOG FR


Fast-twitch Fast-twitch
Fast oxidative glycolytic Fatigue- resistant

liB Fast-twitch FG FF
White Fast-twitch glycolytic Fast-twitch
Fast-fatiguing

50 slow oxidative, FOG fast oxidative glycolytic, FG fast. glycolytic. 5 slow, FR fast, fatigue-resistant. FF fast-fatiguing.

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These characteristics account for the "red" color of such


General Properties fibers and their predominant mode of metabolism,
• Aerobic type I muscle fibers: While varying from muscle which is aerobic, or slow oxidative. (Wheater et aI.,
to muscle, the type muscle I fibers are generally small in 1979).
cross-section, contain abundant mitochondria, and have • Anaerobic (glycolytic) type 1/ muscle fibers: Again, keep­
a large content of myoglobin and a rich blood supply. ing variation of size in mind (depending on the muscle
in question), the type II fibers are typically larger in

- \
cross-section than the type I fibers. They contain few
- \,
)
r�1 mitochondria and little myoglobin, and have a relatively

' '--)
\ poor blood supply. These characteristics account for the
-{
." -' "white" color of such fibers and their predominantly

liB anaerobic mode of metabolism. These muscle fibers are


'1'-- " rich in glycogen and glycolytic enzymes. Anaerobic fi­
bers predominate in muscles responsible for intense but
sporadic contraction such as the biceps and triceps

�l< -. .0 , ) IIA ' - ',


muscles of the arm (Wheater et aI., 1979).

r '\ \____..1 As Frontera (2000) points out, the various muscle fiber type
groupings should be viewed on a continuum with dynamic
properties rather than as static or separate and discrete
Fig.4.9 Cross- section of a human multifidus muscle and incubated
for alkaline ATPase, The muscle had been incubated prior at a pH classes. This continuum is defined by the presence of the
10.5 (x 200 magnification), different isoforms of both the contractile proteins (e.g.,
myosin heavy and light chains) and the regulatory muscle
proteins (e. g., troponin and tropomyosin) (Billeter et aI.,
1981; Billeter and Hoppeler,1994; Heizmann et aI., 1981;
Schiaffini and Reggiani. 1994), The expression of these
proteins is reportedly controlled at the gene level (Moss'
et al. . 1995).

Fiber Type Determination


The histochemical method for distinguishing the various
muscle fiber types under the light microscope is the myo­
fibrillar ATPase stain. It takes advantage of three different
ATPase isoforms. which react differently to specific pH
variations (Cumming et al.. 1994).

• pH 10.5: When the muscle biopsy section (e.g.. 14 m


Fig. 4.10 Acid ATPase with prior incubation at a pH 4.3.
frozen section) is incubated in a basic solution at a pH of
10.5. the subsequent ATPase reaction will stain only the
type II fibers (anaerobic muscle fibers-fast myosin).
,.
, .
with the result showing dark-brown coloration of the
type liB and intermediate brown coloration of type IIA
fibers. The ATPase of type I is inactivated at a pH of 10.5
(Fig.4.9), giving them a pale appearance.
1113 ,; ) • pH 4.3: The reverse is true when a biopsy muscle section
is incubated at a pH of 4.3. In this instance. the type I

I.,.

I, I f'I fibers (slow myosin fibers) stain dark whereas type IIA
fibers stain the lightest and type liB as intermediate
" " '
(Fig.4.10).
.. • pH 4.6: When incubated at pH 4.6, the type I fibers stain
dark whereas type lIB stain in a medium brown color
,
\ while the type IIA fibers remain pale (Fig.4. 1 1).
Fig. 4.11 Acid ATPase with prior incubation at a pH 4.6.

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The physiologic characteristics of the different fiber types


are not as easily differentiated as the ATPase stain may
indicate. since the results of this method may not only
vary but may also be influenced by a pathological condition
that can render the fiber's type indistinct (Cumming et al..
1994). It has therefore become standard practice to take
advantage of the property of the myofibrillar ATPase reac­
tion to show different staining patterns at different pHs and
to perform the reaction on serial sections. following acid
pre-incubation conditions. usually at or around pH 4.3.5
(Cumming et al.. 1994).
The fiber composition in terms of the percentage dis­
tribution of the different fibers ultimately determines the
characteristics of the individual muscle. Fig.4.12 Characteristic "type grouping" predominates in the right
The muscle fibers that are innervated by a single motor muscle fascicle and is less prominent. but present. in the left
fascicle.
neuron make up the fibers of one motor unit. With the
exception of a few sporadic cases and a few transitional
types of fibers. the muscle fibers associated with one motor
unit are usually of the same muscle fiber type. Due to the
presence of various motor units next to each other. the
associated muscle fiber assumes the appearance of a chess­
board pattern (Burke et al.. 1971; Kugelberg and Edstrom.
1968).
Johnson et al. (1973) point out that human skeletal
muscle is subject to great variations. which may explain
the rather large range for "normal values." According to the
same authors. the composition of the erector spinae
muscle. for instance. is by no means uniform; when exam­
ined for the presence of type I fibers. the proportion varied
between 30% and 80%. A similarly large variation was
Fig.4.13 Selective atrophy of the type II muscle fibers.
found when using mean fiber diameter measurements
(Polgar et al.. 1973).
Thus. at least two different samples collected at two Engel (1968) coined the term "type grouping" for the phe­
different time points are needed in order to follow over nomenon. which has been associated with a chronically
time any possible changes in a person's muscle composi­ denervated state (Morris and Raybold. 1971) (Fig.4.12).
tion or the progression in response to particular activities
or possible pathologic processes. Selective Atrophy of One Fiber Type
Atrophy of exclusively one fiber type only is not thought to
be due to typical neurogenic process. This form of atrophy
Pathologic Changes in Muscle Morphology as a Result is thought to be the result of immobilization or disuse or
of Neurogenic Processes underuse of a particular muscle or muscle group (Fig. 4.13).

"Type Grouping" Atrophy of a Large Fiber Group


The stain of a biopsy section reveals rather large. relatively When one fascicle is characterized by atrophic fibers while
uniform groups of one muscle fiber type next to another. the neighboring fascicle is almost normal. one should con­
Denervated muscle fibers are re-innervated by collateral sider the possibility of denervation (Fig. 4.14).
sprouting of the neighboring axons (Harrimann and
Taverner. 1970; Kugel berg et al.. 1970; Grinnell and Herrera. "Target Fibers"
1981; Wernig and Herrera. 1986; Edstrom and Larsson. In the presence of a denervation process. the type I fibers
1987). may assume the appearance of a "target." There is a rela­
The appearance of the fibers grouped by type in this way tively clear and empty central zone that is absent of any
can thus easily be distinguished from the otherwise unaf­ enzyme activity and is surrounded by a dark. strongly
fected. normal-appearing chessboard pattern. Karpati and oxidative ring (middle zone) and a relatively normal outer

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Fig.4.14 Muscle fascicle with atrophied fibers and "type grouping." Fig.4.15 "Target fiber" (arrow). (x 250 magnification).

Fig.4.16 Fig.4.17 "Moth-eaten fibers" (x 200 magnification).


a Core-targetoid fibers (x 50 magnification).
b " Core-targetoid fibers (x 200 magnification).
• Target fibers.

peripheral zone. Again the type I fibers are more frequently "Split Fibers"
involved. showing this type of pattern as a result of dener- On occasion the muscle fibers can undergo splitting.
vation. However. a similar appearance has been described Extensive splitting can cause a large muscle fiber to be-
for fibers during re-innervation after initial denervation come divided into small subfibers. As a normal variant.
(Dubowitz. 1967) (Fig.4.15). such changes have been observed in particular at the
myotendinous junction. Similar changes have been ob­
"Core-targetoid Fibers" served in progressive muscle dystrophies as well as
Primarily type I fibers show this type of stain. again due to chronic denervation processes (Hall-Craggs and Lawrence.
denervation processes (Fig. 4.16). The central core does not 1970) (Fig. 4.1 8).
stain. however. Bagnall and co-workers (1984) studied biopsy sections
from the multifidus muscle in patients who were known to
"Moth-eaten Fibers" have a disk herniation. They demonstrated no difference
The "moth-eaten" appearance is due to aberrations in the between the side of disk herniation and the opposite "nor­
intermyofibrillar network. An oxidative enzyme reaction is mal" side and thus used these findings as the "nollllal"
able to demonstrate this histochemically. The "moth­ control. Mannion et al. (1997) also did not find any patho­
eaten" character has only been found in type I fibers. and logic changes in the musculature. in contrast to the reports
hence this pattern has been seen in various types of myo­ of Mattila et al. (1986) and Zhu et al. (1989).
pathy. The finding is rather nonspecific. however (Fig. 4.17). Sirca and Kostevc (1985) compared cadaveric biopsy
sections obtained from the multifidus muscle of 21 men

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with those of 12 men and five women obtained during disk


herniation surgery. They found that the fiber diameter was
smaller in the biopsy samples obtained during live surgery
than in those obtained at autopsy. The percentage fiber
composition was similar in both study groups.
Mattila et al. (1986) compared biopsy samples of the
multifidus muscle obtained from a group of 41 patients
who had a demonstrated disk herniation with 12 control
subjects (autopsy). In both groups the type II fibers were
prominently smaller than the type I fibers. The disk hernia­
tion group also had findings of core-targetoid and/or "moth­
eaten" fibers among the type I fibers. Since the control
samples did not show any of these findings, they were
Fig.4.18 "Split fibers" after Hall-Craggs and Lawrence (1970) as
considered to be the result of pathologic changes. Type
seen in this basic ATPase stain and neighboring "type grouping"
grouping was found in only a few cases. ( x 160 magnification).
Zhu et al. (1989) studied the biopsy samples of 22 pa­
tients who were undergoing disk herniation. The sample
was obtained from the erector spinae muscle on the same multifidus muscle (54.1 %, Jorgensen et aI., 1993; 54.9%,
side as that of disk herniation (L3-S1). Eighteen of the 22 Johnson et al. 1973; 66.6%, Sirca et a!. 1985; 60.6%, Mattila
patients revealed a typical atrophy of fiber type II, three of et al. 1986; and 57. 4%, Rantanen et al. 1994).
whom had type liB atrophy only. The type II atrophy corre­ Mannion et a!. ( 1997 a) report that the percentage con­
lated well with the patient's age and symptom duration. tribution of type I fibers in sections obtained from patients
The atrophy of the type II fibers was significantly higher in who had undergone surgery was approximately 51%, while
patients older than 40 years and those who had a long that in the control group was 66%. Mannion et al. (2000)
duration of symptoms (longer than one year). In addition report the percentage contribution of type I fibers for pa­
to the atrophy, a number of pathologic changes were ob­ tients with low back pain as 65% for men and 73% for
served upon histochemical examination. No significant dif­ women.
ferences were demonstrated between biopsies obtained at Fiber composition in samples obtained from the multi­
different segmental levels. fidus muscle of the lumbar spine did not reveal a clear
After these studies in 1993, Rantanen and co-workers correlation between patient age and percentage fiber com­
reported their findings of biopsy samples from the same position. The older the patient, the greater the proportion
patient at two different time points (Rantanen et aI., 1993). of type I fibers at the expense of type lIB fibers. Mannion et
The first sample was obtained at the time of disk herniation a!. (2000) found that with increasing age there is a decrease
surgery with a total of 18 patient biopsy samples harvested in fiber size, especially type II, while there is an increase in
from the multifidus muscle. The second biopsy samples the percentage of type I fiber. Comparing the different
from the same muscle were obtained from the same per­ published data, it appears that while the type lIA fiber
sons 5 years later. Interestingly, the muscle biopsy exami­ composition was higher than the type liB in healthy sub­
nations revealed a change in pattern in those patients who jects as well as those found in autopsy, the opposite was the
had later become pain-free and who had been satisfied case in samples obtained from symptomatic patients. Uhlig
with their surgical outcome. et a!. (1995) examined biopsy samples obtained in the
Evaluation of the multifidus muscle showed a greater cervical spine and found that the type lIB fiber type was
proportion of type I fibers (56 .7%) than type II fibers. Ac­ higher in patients with respect to longer symptom dura­
cording to Weber (1995) the proportion of type liB fibers tion. The same was reported by Mannion et al. (2000) in
was higher than that of type IlA fibers (24.6% and 17.1%, patients with nonspecific low back pain.
respectively), but this difference was not statistically sig­ One study reported that the ratio of type lIB to type A
nificant. There was no significant difference in fiber com­ fibers was increased in patients who had been immobilized
position between men and women. Mannion et al. (1997 b) (Haggmark and Ericksson, 1979). It is therefore plausible
found no differences in the percentage of fiber types ac­ that the relatively higher proportion of type liB fiber type in
cording to race or sex; but there was a significant difference our studies and those of other workers may be the result of
in relative size of the type I and type II fibers, such that immobilization/disuse and thus decreased loading on the
women had a greater proportional area of the muscle back musculature.
occupied by type I fibers. The percentage of type I was The study reported by Johnson et a!. (1973) found a
similar to values reported from autopsy samplings of the relatively greater percentage of type liB than of type IIA

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Neurophysiology of the Joints and Musdes

fibers in six young, healthy subjects. This finding may Since these findings are nonspecific and have been
reflect the study subjects' ages, as they were between 17 found in a number of pathological conditions, their patho­
and 29 years old. According to our own studies, the per­ genesis has not been unequivocally established. Fiber atro­
centage of type liB fibers is reduced with advancing age, phy has been shown as a result of disuse or immobilization
while that of type I and type IIA fibers increases (Mannion (Brooke and Kaplan, 1972) as well as denervation (Carpen­
et aI., 2000). A similar finding had been presented in a large ter and Karpati, 1984; Dubowitz, 1985; Jennekens, 1982;
study that used the vastus lateralis muscle as a source of Lindboe and Presthus, 1985). Other muscle diseases have
the biopsy (Larsson et aI., 1978). also been invoked (Carpenter and Karpati, 1984; Dubowitz,
Zhu et al. (1989) examined the multifidus muscle via 1985).
biopsy samples obtained from patients who were under­ "Core-targetoid" fiber changes have been observed in
going disk herniation surgery. They differentiated their such conditions as ischemia (Heffner, 1978), polymyalgia
samples according to two age groups and found an increase (Carpenter and Karpati, 1984; Dubowitz, 1985), denerva­
in type I fibers at the expense of type liB fibers with tion (Carpenter and Karpati, 1984; Dubowitz, 1985), or as
advancing age; however, the differences were not statisti­ result of muscle training (Brooke and Kaplan, 1972).
cally significant. Type II fiber atrophy was observed in biopsy samples
Interestingly, Rantanen et a!. (1994) did not detect any obtained from control subjects in studies presented by
significant difference in the examination of samples of the Mattila et a!. (1986) and Mannion et al. (1997b). The ques­
multifidus muscle of 21 individuals between the ages of 23 tion arises whether the observed changes should be inter­
and 65 years. Thus, we believe that it is important to preted as a "normal" finding in a "healthy" population or
determine the presence or absence of back pain in subjects whether this is the expression of insufficient use of the
whose samples would serve as control, and the lifestyle of back muscles and the relatively sedentary activity of the
the control subjects should be included in the study profile. "modern" population. Mannion et a!. (1997b) suggest that
The majority of these examinations of the back muscles of the data from their study could be of use in assessing
"healthy" persons were performed in the Scandinavian deviations from the norm in clinical material acquired
countries. It is known that there many people regularly from patients with various upper and lower back disorders.
participate in such activities as cross-country skiing, which The relationship established between body size and
utilizes the back musculature and therefore may influence muscle fiber size could be employed to evaluate the degree
the "normal" control group. It is possible that similar ca­ of atrophy in muscle samples collected from individuals
daveric samples obtained from persons who lived else­ with widely differing anthropometry. The same authors
where (e. g. Switzerland) might have produced different (Mannion et aI., 1997b) conclude that when assessing the
results. extent of any pathological change in the muscle of low
A central questions, then, remains whether the increase back pain patients, it seems clear that: (1) sex cannot be
of type I fibers at the expense of type liB fibers is the same disregarded; and (2) "atrophied" (by the criteria used to
or similar in patients who experience low back pain and assess other muscles) type II fibers are not necessarily
those who remain nonsymptomatic but are relatively in­ abnormal for the erector spinae muscle, particularly in
active. Both groups are thought to share a similar lack of women.
use of the back muscles. Rantanen et al. (1993) proposed that the "modern indi­
It would appear that only a few of the biopsy samples vidual" uses his or her back muscles so sparingly that the
obtained in the various studies revealed no pathologic different muscle fibers, in particular the type II fibers, have
changes. The most frequent finding was that of type [J fiber no chance of developing their normal fiber caliber. This
atrophy (40% in symptomatic patients) and a relative in­ view appears to be supported by an earlier study by Polgar
crease of "core-targetoid" fibers in 29% of symptomatic et a!. (1973), who found that the erector spinae muscles of
patients. five healthy men contained a type II fiber diameter that was
Both Ford et a!. (1983) and Rantanen et a!. (1993) report larger than usual (53.6 [lm). Further delineation would be
type II atrophy and "core-targetoid" fibers in multifidus required, however, and it would be interesting to see the
muscle obtained from patients with disk herniation. While comparison between inactive individuals and highly active
Ford et al. interpret this as a variation of normal muscle athletes.
fiber, Rantanen et a!. (1993) believe that these changes are The study presented by Rantanen et a!. (1993) presents a
actually disease specific. Zhu et al. (1989) share the latter number of findings that merit mention in this context.
view as his group also found type II fiber atrophy in 18 of 22 Patients who underwent surgery for disk herniation were
patients with demonstrated disk herniation. Furthermore, subjected to comparative biopsy studies with the initial
they believe that the atrophy was not only due to disuse or sample taken at the time of surgery and the second sample
immobilization and bed rest, but also to denervation. 5 years after. Those patients who had a "positive" surgical

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outcome, that is, improvement after surgery, were found to Muscle Receptors
have a significant increase in the type II fiber size, In other
words, while in pain, patients in general revealed type II Skeletal muscles contain the following five types of recep­
fiber atrophy at the time of surgery. Similar atrophy tors:
patterns were found 5 years later only in those persons
who reported either unresolved and continued pain or • Muscle spindles.
those who were dissatisfied with their operative outcome. • Golgi tendon organs.
Thus it would be reasonable to assume that the decrease in • Pacinian corpuscles.
the type II atrophy in the "positive" (improved) group • Free nerve endings (nociceptors, type IV receptors).
might reflect a successful result with medical training ther­ • Mechanoreceptors (type III proprioceptors).
apy. On the other hand, the continued presence of type II
atrophy in the "negative" (poor outcome) group may be the The two principal "muscle receptors" are the muscle spin­
result, at least to some extent, of immobilization, disuse, or dles and the Golgi tendon organs. They will be described in
pain, or of a combination of these and potentially other detail in this section. A description of the three-dimen­
factors. sional free nerve endings and the type III mechanorecep­
Mannion et a!. (1997 a) come to different conclusions. tors, which are principally located at the tendon-bone
They found that there is a greater fast-twitch, glycolytic junction, was presented earlier.
profile for the lumbar spinal musculature of patients with
low back pain than for that of patients classed as normal
Muscle Spindles
controls (of similar sex, age, and size). They conclude that
this is likely to have a detrimental effect on the fatigue Distribution and location
resistance of the back muscles, They further conclude that Morphologic studies of the muscle spindles (Richmond and
while it cannot be ascertained whether the abnormality Abrahams, 1979) indicate a rather large variation in num­
precedes or follows the onset of low back pain, once this is ber, distribution, and location. A pronouncedly high con­
identified attempts should. be made to remedy the situa­ centration of spindles is found in muscles thought to be
tion with exercise therapy to bring the fiber type character­ responsible for fine and precise movements, such as the
istics more in line with that displayed by pain-free controls hand and eye muscles. In the spine, the small suboccipital
(Mannion et a\., 1997 a, 2000). muscles, for instance, have approximately 150-200 muscle
In summary then, an increased percentage of type 11 spindles per gram of muscle tissue. There is also an excep­
fibers is often found in symptomatic patients and type 1\ tionally high concentration of muscle spindles in the para­
atrophy appears to increase with advancing age. It further spinal musculature, such as the intertransverse muscle of
appears that the type II atrophy may be a reversible phe­ the cervical spine, where it is not uncommon to find
nomenon, especially when patients are able to return to 200-500 spindles per gram of muscle tissue. In contrast,
pain-free and normal movement. Whether the type II atro­ the total number of spindles is comparatively small in the
phy in the back muscles can be reversed through specific larger muscles responsible for gross movement, such as the
exercise training routines and by increasing one's physical rectus femoris muscle, which has only 50 muscle spindles
patterns should be the subject of further studies (Weber et per gram of muscle tissue. Thus muscle spindles are infre­
al.,1996). quently present in biopsies from large limb muscles, where
At this point it is unknown whether intramuscular pres­ they may be confused with pathological features (Cum­
sure can alter or change fiber composition in the paraspinal ming et aI., 1994).
musculature. It has been reported that increased intramus­ In terms of their distribution, there is a preponderance
cular pressure may co-exist with back pain or may lead to of muscle spindles in the postural, oxidative slow-twitch
chronic compartment-type syndrome of the paravertebral muscles (Richmond and Abrahams, 1979). Arguably, this
muscles (Konno et aI., 1994). fact may support the notion that the postural muscles
With regard to the relationship between muscle capil­ play a particularly important role in spinal mechanics
lary supply and fiber size or fiber type, Ahmed and co­ when subjected to abnormal loading conditions. As noted
workers (Ahmed et aI., 1997) calculated the local capillary previously, there is a greater proportion of slow-twitch
to fiber ratio or density based on area, rather than number fibers in those muscles whose primary task is that of main­
of fibers. Their results suggest that, in human skeletal taining posture.
muscle, capillary supply is primarily scaled according to From a clinical perspective, and this is mostly empirical
fiber size and is relatively independent of fiber type. Uanda, 1986) there is the notion that the postural muscles
tend to shorten in response to a joint-related dysfunction.
This is in contrast to the phasic muscles with a high density

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ming et aI., 1994). The muscle spindles are imbedded

8 r::
within the regular muscle bulk in a parallel arrangement
with respect to their contractile counterparts, the extra­
fusal muscle fibers (Freeman and Wyke, 1967). Muscle
contraction is characteristically accompanied by shorten­
ing of the extrafusal muscle fibers, which in turn reduces
the tension in the noncontractile portion of the muscle
Decreased tension
spind Ie (Fig.4.19). However, the length of the muscle spin­
dle is continually adjusted in order to register muscle
Stretch
--. EFMF length from moment to moment. Both the extrafusal and
intrafusal fibers are subjected to increased tension when
the muscle is stretched (Brodal, 1981; Simons, 1976a).
IFMF

Increased stretch Goigi Tendon Organs

The Golgi tendon organs are clusters of large myelinated


Fig.4.19 Schematic representation of muscle spindle function.
nerve fibers (12-18 m) (Cooper and Daniel, 1963; Schoultz
EFMF Extrafusal muscle fibers
IFMF Intrafusal muscle fibers and Swett, 1972). They are typically found at the muscle­
tendon junction where they terminate with free endings
between the collagen fibers of the tendons. In contrast to
the muscle spindles, the Golgi tendon organs are arranged
in series with the extrafusal muscle fibers. This important
anatomic difference is mirrored in the functional proper­
ties of these two receptors. The tendon organs primarily
detect any changes in tension and are activated not only
upon muscle contraction but also upon relaxation. In other
words, the Golgi tendon organs function primarily as ten­
sion receptors, whereas the muscle spindles first and fore­
most register changes in muscle length (Granit, 1955, 1975).

Motor End Plates

Fig.4.20 Histologic section of motor nerves and their terminations


A motor neuron and all the muscle fibers it innervates
in the motor end plate (dark brown).
constitute a motor unit (Cumming et al., 1994). The alpha
a The motor end plates are arranged along a line or within a
certain lone. motor nerve fibers terminate at the muscle through a
b This macroscopic view of the medial muscle group of the arm single motor end plate. Typically the motor end plates are
demonstrates how the end plates are arranged along superficial located near or in the center of the extrafusal muscle fibers
rows which show up in this photograph as dark blue lines. The
they innervate. The arrangement of the end plate-muscle
course of the row or zone of end plates depends on the muscle
junctions can be visualized both microscopically and mac­
Fiber direction.
(With kind permission of Dr. J. (homiak, Prague) roscopically by various means (Fig.4.20). In the aggregate,
the motor end plates form essentially a band or zone that
helps demarcate the muscle. With a simple esterase stain,
of fast-twitch fibers, which tend to become weak before these markings are readily discernible to the naked eye on
they shorten in response to dysfunction. the muscle's surface. Using an indigo stain will render the
motor end plates and myotendinous junctions visible as
Anatomy and Function blue dots, and they can also be easily noted on the muscle's
The muscle spindles consist of 3-20 slender specialized surface (Fig.4.21). Since the location of the motor end
muscle fibers. which have been specifically termed the plates appears to remain relatively fixed throughout life,
intrafusal muscle fibers. They are enclosed for most of their the examination of fetal muscles is a preferred method of
length by a connective-tissue capsule. Normal features of study (Chomiak et al.. 1995).
these structures are great variability in intrafusal fiber size In clinical practice. there are a number of situations that
and histochemical type, centralized myonuclei, high ester­ require a thorough understanding of the localization of the
ase activity. and prominent nervous-tissue elements (Cum­ various motor end plates. For instance, the electromyogra­

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Functional Pathology of Muscle

pher is very careful in localizing the specific motor end


plates for particular electrodiagnostic needle studies. Cer­
tain kinesiologic studies require specific placement of the
electrodes for motor-evoked potentials. Most recently. the
injection of botulinum toxin into areas of the myoneural
junctions requires a good understanding of their location in
a particular muscle.
To date there have been no studies able to correlate the
motor end plate function or changes and the myofascial
trigger points described by Simons (1983a. b). and Travel!
and Simons (1992).

Fig.4.21 Schematic representation of the different types of pin­ Alpha-Gamma Coactivation


nate muscles according to the course of the motor end plates.
a Nonpennate muscle with parallel muscle fiber direction.
b Nonpennate muscle with oblique muscle fiber direction.
Despite its complexity. this mechanism is presented here

c Simple pennate muscle. because of its importance in understanding the function of


d Bipennate muscle. the alpha and gamma motor neurons and their role in
e Multipennate muscle. manual medicine (Granit, 1955.1975). A graphic represen­
tation is reproduced in detail in Fig.4.22 (after Hassler.

Fig.4.22 Schematic repre­

Normal circuit sentation of mechanisms re­


sponsible for control of
. Muscle tension
muscle length (circuit on the
right) and muscle tension
(circuit on the left). (After
Hassler, 1981.)

t-
Ib

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Neurophysiology of the Joints and Muscles

1981). In the diagram, the right half represents the circuit muscle tension, even under the influence of external
responsible for reflexive muscle length changes, while the stretching forces, is regulated by a feedback mechanism
left half represents events associated with the circuit of between the regular stretch reflex (originating from the
muscle tension control and external stretching force appli­ secondary endings) and the so-called relief reflex (Hassler,
cation. 1981).
Components of the reflex arc of the phasic propriocep­ Rethelyi and Szentagothai (1973) observed that the af­
tive reflex include the nuclear bag and the intrafusal ferent fibers originating from the muscle spindles send off
muscle fibers, which undergo contraction when stimulated collaterals to more than one spinal segment at the dorsal
by the gamma-1 neurons. This causes the noncontractile root level. This is particularly helpful when considering the
central portion of the muscle spind Ie, the nuclear bag, also principles involving the alpha-gamma co-activation sys­
to become stretched. Subsequently, the surrounding spiral tem (Brodal, 1981). This information may have clinical
endings of the la fibers (the primary or annulospiral end­ relevance as it may help explain, at least in part, such
ings) also become distracted. This mechanism is responsi­ entities as the "facilitation" of dysfunctions, or if unre­
ble for the proprioceptive reflex, which, via the la fibers and solved, the maintenance of a segmental (somatic) dysfunc­
the direct reflexive collateral branches, connects with the tion and the various spondylogenic reflex syndromes. Thus,
alpha-1 motor neurons, resulting in contraction of the it would appear that the afferent information from one
extensor muscles. By way of innervation through the muscle spindle is able to affect motor neurons associated
gamma-1 system it is assured that the very sensitive nu­ with more than one or several spinal segments (Brodal,
clear bag can be "reset" in response to a shortened sur­ 1981 ).
rounding muscle, which is then automatically maintained
through the proprioceptive reflex. The strength of the pha­
sic proprioceptive reflex is directly dependent on the ex­ Postcontraction Sensory Discharge
ternal stretching force, as well as on the activity of the
gamma-1 system. Several authors have investigated the rol.e of the postcon­
traction sensory discharge in clinically shortened postural
Circuit for Muscle Tension Control or tonic muscles (Brown et aI., 1970; Eldred et aI., 1976;
Upon stimulation of the tonic gamma-2 fibers, the intra­ Hnik et aI., 1973). Buerger (1983) suggests that this phe­
fusal muscle fibers of the thin nuclear chain fiber will nomenon may explain some of the therapeutic effects of
contract. The spindle afferents of the smaller size (type II) various manual medicine techniques.
fibers terminate primarily on the polar segments of the Single-fiber studies using single annulospiral endings,
nuclear chain fibers via the secondary or flower spray as well as studies from the entire root portion, have indi­
endings (II in Fig. 4.22). External stretch induces these end­ cated that a tetanic stimulation of a single muscle spindle
ings to fire; this is ultimately relayed to the alpha-2 motor or its gamma-efferent fiber can cause an increased dis­
neurons in the anterior horn cells via the afferent type II charge pattern at the respective annulospiral ending. A
fibers and their multiple synapses at the spinal cord level. It shortening in the respective muscle spindle led to a de­
is these alpha-2 motor neurons that cause the slow pos­ crease in discharge. Rapid overstretch of the involved
tural muscles to contract. The length of the postural muscle spindle, however, prevented the discharge pattern
muscles is maintained as long as the nuclear chain fibers otherwise seen upon tetanic gamma stimulation.
are held at a particular length through the influence of the The clinical relevance of these experimental observa­
gamma-2 neurons. tions, especially as they relate to the mechanism of short­
Besides the feedback provided through the tonic stretch ening of the postural muscles, cannot be conclusively as­
reflex, another major regulatory component, if not the certained at this time. However, one may postulate that the
singularly decisive component of muscle tension, is the postcontraction sensory discharge phenomenon may
Golgi tendon organ. Originating from the tendon organs somehow be involved in the event of muscle shortening
are fast Ib fibers that convey the incoming information to and/or with the process of transformation of the fast­
the spinal cord and, by way of several interneurons, have twitch fibers to slow-twitch fibers.
an inhibitory effect on both the alpha-l and aJpha-2 motor
neurons. This leads to the inhibition of the contraction of
the postural muscles via the alpha-2-efferent neurons, thus Nociceptive Muscle Af ferents; Muscle Pain and
countering the effect of the tonic stretch reflex (a "relief Regulation of Muscle Tone
reflex," in a sense). The alpha-1 efferent motor neurons
terminate on those contractile muscle fibers that are in­ Reviewing the above, it is the la fibers that supply the
volved in the phasic extensor action. The conclusion is that primary muscle spindles, and it is the Ib fibers that inner­

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Functional Pathology of Muscle

vate the Golgi tendon organs. In addition. the muscle spin­


dles are further innervated by type II muscle afferents,
which have appropriately been referred to as the secon­
dary spindle afferents.
However, to date, very little is known about the three­
dimensional free nerve endings of the nociceptors associ­
ated with muscles and their afferent circuits. One would be
safe in assuming that at least one of the roles of the free
nociceptive nerve endings is to register and respond to
actual tissue damage or toxic stimuli that could potentially
lead to tissue damage. Studies by Mense (1977) indicate
that the muscle nociceptors are present relatively incon­
sistently. They can be activated either mechanically (hyper­
algesia associated with pressure) or chemically (bradyl<i­
nin, potassium, serotonin, among other agents). They have
also been activated upon prolonged state of muscle con­
traction or as a result of ischemic changes. According to
Graven-Nielsen and Mense (2001) and contrary to former
belief, the sensitization of muscle is not an unspecific pro­
cess. These authors further believe that the sensitization
process is caused by endogenous algesic substances bind-
ing to highly specific receptor molecules in the membrane Fig.4.23 Vicious cycle resulting in an increase in muscle tone upon
of the nociceptive ending. The sensitization process by chronic irritation of the small nOCiceptor afferents from skeletal
endogenous substances that are likely to be released dur­ muscles. (After Schmidt et al., 1981.)
ing trauma or inflammatory injury is probably the best-
established peripheral mechanism for muscle tenderness
and hyperalgesia (Graven-Nielson and Mense, 2001). neurons at the spinal cord level. This study further dem­
Graven-Nielsen et al. (2004) evaluated painful and non­ onstrated that this type of transmission occurs with note­
painful pressure sensations from human skeletal muscle by worthy intensity and is by no means only a marginal oc­
comparing sensations when: (1) the skin was anesthetized; currence.
and (2) the skin was anesthetized in combination with a Mense (2003) describes the continuum of the involve­
block of large-diameter muscle afferents. Their data show a ment of nociceptors peripherally and their influences on
marginal contribution of cutaneous afferents to the pres­ spinal cord and medullary level changes that lead to hyper­
sure pain sensation while there is relatively more depen­ excitability and hyperactivity, and thus spontaneous pain
dence on the contributions from deep tissue group 111 and and hyperalgesia. Due to central sensitization-especially
IV afferents. Furthermore, the same authors note that a in light of the spinal cord's demonstrated neuroplastici­
pressure sensation can be elicited from deep tissue, prob­ ty-one must differentiate between short-term or one­
ably mediated by group III and IV afferents involving low- time pain and pain that extends over time and is associated
threshold mechanoreceptors. with changes from functional changes to structural
Most recently, Gibson et al. investigated referred pain changes.
and hyperalgesia in human tendon and muscle belly tissue Based on the information provided by the laboratory of
(Gibson et aI., 2006). I n the 18 subjects, they found that the Schmidt et al. (1981), we may theorize that the small­
proximal tendon bone joint junction and tendon sites are caliber muscle afferents can have a profound influence on
more sensitive and susceptible to sensitization by hyper­ the overall degree and the extent of muscle tone in both in
tonic saline than the muscle belly site. Furthermore, the static and dynamic situations.
same authors propose that there may be site-specific The findings of these animal studies appear to indicate
central changes reflected in the differences in the results that the stimulation of the nociceptive muscle receptors,
regarding sensitivity and summation over time. either as a result of pain or due to some chronic or recur­
Schmidt et al. (1981) studied the alpha motor neuron rent irritation, can produce a permanently increased
system in response to painful muscle stimulation in ani­ muscle tone via the interaction with the small-caliber
mals. These authors found that in response to painful stim­ muscle afferents of the type III and type IV and the gamma
uli the small-caliber muscle afferent fibers (nociceptive loop.
afferents) have direct access to the alpha and gamma motor

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Neurophysiology of the Joints and Muscles

At this time it can be argued that this mechanism may ciates (2006), Maeda et al. 2007, and Skyba et al. (2003),
play a specific role in humans as well, especially in relation­ describe a reduction of hyperalgesia through joint manip­
ship to the so-called localized "muscle spasm" that is often ulation or the use of high-frequency TEN S .A recent clinical
associated with a segmental (somatic) dysfunction. This study (Moss et al. 2007) reports that mobilization of an
mechanism may also explain reports of progressive muscle osteoarthritic knee joint is associated with both local and
damage caused by chronic hypertonic muscles or spasms widespread hypoalgesic effects.
(Fassbender, 19 80) . Thus, with the arrival of new investigative techniques at
Figure 4.23 graphically illustrates the vicious cycle that the molecular level (e. g. biomarkers) and ever-refined clin­
is initiated by some primary disturbance and activates and ical diagnostic possibilities (e. g. fMR (2003), greater reso­
perpetuates the firing of the various nociceptive receptors lution of MRI and dynamic applications, etc.) new venues to
in skeletal muscle, subsequently invoking transmission via study physiologic mechanisms attributable to manual
the associated small-caliber nociceptive afferents. This in medicine have opened up and are expected to further our
turn activates the gamma loop, ultimately increasing understanding of what really happens during and after
muscle tone via the alpha motor neuron through the la treatment.
and II afferents. Ultimately it may be possible to connect the dots," that
is the biomechanical principles, neurophysiologic, humoral
and hitherto-unknown pathways: all of them within one
What's on the Horizon - When Manual functional unit, the human body.
Medicine and Molecular Medicine Meet
"What's on the Horizon" - Further Reading
Based on the recent advances in the human genome se­
quencing and proteomics, new diagnostic and therapeutic Degenhardt BF, Darmani NA, Johnson]C (2007) Role of osteo­

opportunities are anticipated for individualized orthope­ pathic manipulative treatment in altering pain biomarkers:
a pilot study. JAOA. 107:387-400.
dic/musculoskeletal management of various disorders, all
Evans CH, Rosier RN (2005) Molecular biology in orthopaedics:
the while both surgical and nonsurgical decisions will in­ the advent of molecular orthopaedics. J Bone Joint Surg Am.
creasingly accommodate molecular criteria (Evans et al. 87(11 ):2550-2564.
2005). Maeda Y, Lisi TL, Vance CG, Sluka KA (2007) Release of GABA

In the field of manual medicine, Degenhardt et al. (2007) and acti vation of GABA(A) in the spinal cord mediates the
effects of TENS in rats. Brain Research. 1136(1):43-50.
report that various nociceptive (pain) biomarkers were
Malisza I<L, St roman PW, Turner A, et al (2003) Fun ct ion al MRI
altered in response to osteopathic manipulative treatment of the rat lumbar spinal cord involving painful stimulation
(OMT) while the degree and duration of these changes and the effect of peripheral joint mobilization. J Magn Res
were greater in subjects with chronic LBP than in control Imag.18(2):152-159.
subjects without the disorder. Moss P, Sluka I<A, Wright A (2007) The initial effects of knee
joint mobilization on oste oa rthritic hyperalgesia. Manual
In another recent study, a single spinal manipulation
Therapy. 12(2):109-118.
therapy (SMT) application to the thoracic spine was dem­ Pavlov VA, Wang H, Czura CJ, et al.(2003) The Cholinergic Anti­
onstrated to down-regulate inflammatory-type responses Inllammatory P a thway: A Missing Link in Neuroimmuno­
as observed by a reduction of proinflammatory cytokine modulation. Mole Med. 9: 125-134.

secretion (Teodorczyk-Injeyan 2006).


Skyba DA, Radhakrishnan R, Rohlwing JJ, et al. (2003) Joint
manipulation reduces hyperalgesia by activation of mono­
While not mentioned specifically in the seminal papers
amine receptors but not opioid or GABA receptors in the
on the cholinergic anti-inflammatory pathway - a newly spinal cord. Pain. 106(1-2):159-168.
described neural circuit thought to be involved in cytokine­ Sluka I<A, Skyba DA, Radhakrishnan R, et al.(2006) Joint mobi­
dependent immunomodulation (Pavlov et al. 2003, Tracey lization reduces hyperalgesia associated with chronic
2007), it stands to reason, that manual medicine interven­
muscle and joint inflammation in rats. J Pain. 7(8):602-607.
Teordorczyk-Injeyan JA, Injeyan HS, Ruegg R (2006) Spinal
tions, like other complementary approaches, may play a
manipulative therapy reduces inflammatory cytokines but
role in central mechanisms that modulate systemic and/or not substance P p roduc tion in normal subjects. J Manipu ­

peripheral inflammatory responses. lative Physiol Ther. 29(1): 14-21.


Based on their extensive research experience in inves­ Tracey I<J (2007) Physiology and immunology of the cholinergic
tigating hyperalgesia using animal models, Sluka and asso­ anti-inflammatory pathway; J Clin Invest.117:289-296.

98

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5 The Pharmacologic and Psychologic Treatment

of Chronic Pain

Understanding Pain Mechanisms process following tissue damage in which chemical medi­
ators emerge (e. g., histamine, serotonin, bradykinin, pros­
Several aspects should be considered in pharmacologic and taglandins, ATP, H+, nerve growth factor, TNF-a, endothe­
psychologic treatments of pain that are related to the mod­ Iins, interleukins). These chemical mediators, frequently
ulation of nociceptive impulses or signals. In addition, in referred to as "inflammatory soup" (Besson, 1999; Scholz
the case of chronic pain, neither pharmacologic nor psy­ and Woolf, 2002), act on free nerve terminals and generate
chologic treatment, employed in isolation, leads to satis­ an action potential (i. e., nociceptive impulse or signal). A
factory results for patients. Based on this clinical experi­ complex reaction of small vessels from the surrounding
ence the combination of pharmacologic and psychologic tissue cells also occurs in the inflammatory tissue (e. g.,
treatment of chronic pain is usually the best choice. For mastocytes) to activate or to modify the stimulus response
these reasons pharmacologic and psychologic aspects of of nociceptor afferents. In summary, tissue damage, due to
pain treatment are discussed in the same chapter. trauma or inflammation, initiates biological processes re­
Some knowledge of the basic mechanisms of pain is sponsible for generating the nociceptive impulses or sig­
necessary to understand the possibilities of pharmacologic nals. Acute pain is therefore considered to result from
and psychologic treatment of pain. It is important to under­ noxious (i. e., potentially harmful) messages are derived
stand the molecular mechanisms involved in generating from the activation of free unmyelinated or thinly myeli­
impulses or signals, referred to as nociception, and the nated terminals found in cutaneous, muscular, and joint
processes of translation and modulation of these impulses tissues and in certain visceral structures (Besson, 1999).
in the central nervous system, in particular the complex Finally, different mechanisms in the peripheral or central
processes of modulation that may be crucial to chronic pain nervous system have to be considered for neuropathic pain
development. A comprehensive summary of the complex (Fields et aI., 1998). Sensitized nociceptors may induce
processes involved in generating and experiencing pain is changes in central processing, possibly leading to spinal
beyond the scope of this chapter. Several recent reviews cord hyperexcitability by which input from mechanorecep­
concern the biological basis of pain, and the interested tors by the A -fibers (i. e., touch) is perceived as pain. This
reader is encouraged to consult some of these (e.g., Besson, phenomenon explains essential features of neuropathic
1999; Julius and Basbaum, 2001; Scholz and Woolf. 2002. pain such as hyperalgesia (intensity of pain being higher
Only a rough summary of the mechanisms will be provided then expected) and allodynia (pain that is perceived due to
here. an influence which is usually not perceived as pain, e. g., a
slight blow on the skin). Reorganization in the dorsal horn,
considered to result from C-fibers degeneration, seems to
Pain Mechanisms be responsible for allodynia and is provoked by the activity
of A -fjbers. Furthermore, following nerve lesion in partic­
Three different mechanisms of pain need to be considered: ular, the sympathetic system may interact with spinal af­
nociceptive, inflammatory, and neuropathic pain (Scholz ferent neurons, further sensitizing nociceptors (Fields et aI.,
and Woolf, 2002). Nociceptive impulses or signals originate 1998; Baron, 2000).
from the electrical activity (action potential) of the periph­ One of the central mechanisms in the generation of pain
eral terminals of unmyelinated C-fibers and thinly myeli­ impulses that has been studied in great detail (Fig. 5.1), and
nated AS-fibers. Although no identifiable anatomical struc­ is best understood, is the synthesis of prostaglandins. Be­
ture in the periphery deserves the term receptor, these cause this process considerably affects pain treatment,
fibers are considered to contain receptors that are indeed some aspects are briefly mentioned here.
ion channels sensitive to mechanical stimuli, hydrogen Damage to the cell's phospholipid membrane leads to a
ions, cold, or heat. Under circumstances potentially danger­ release of eicosanoids (e. g., free arachidonic acid), which
ous for tissue, these factors may generate a nociceptive are metabolized as shown in Figure 5.1. P rostaglandins are
impulse or signal, which is an action potential perceived synthesized from phospholipids during this metabolism. As
as pain. This pain is referred to as nociceptive pain. Inflam­ indicated in Figure 5.1. the enzyme cyclooxygenase (COX)
matory pain, in contrast, is the result of a more complex plays a central role in this process. It is important to note

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The Pharmacologic and Psychologic Treatment of Chronic Pain

Fig. 5.1 Biosynthesis of eico­


sanoids. (Adapted from Brune
Membrane phospholipids
and Hinz. 2001.)
Lipoxins
Phospholipase A2 1 lXA.
Free arachidonic acid -15-HPElE -15-HETE
1 O(B.

Cyclooxygenase -t= NSAlDs 5-Lipoxygenase


I

Cyclic 5-Hydroperoxy­
endoperoxides eicosatetraenoic acid

ILl . ! 5-Hydroxy­
eicosatetraenoic acid
PGE, PGD, lXA, PGI, LTB. LTC.
1 1 1 1
PGF2 lXB, 6-keto- LTD.
PGF,Cl 1
LTE.
Prostaglandins Thromboxanes ProstacyC/ins Leukotrienes

that various compounds emerge in the process of metabo­ offered a framework that contributed to the comprehen­
lism of phospholipids. Some of these are important for sive understanding of how chronic pain can develop. This
organisms' function (e. g .. renal flow. function of the endo­ theory works with anatomical structures and uses a so­
thelium and gastric mucosae). Others, such as prostaglan­ called gate-system in the dorsal horn of the spinal cord, in
dins, are involved in inflammatory reactions. which processing and modulation of the nociceptive im­
Prostaglandins play a major role in acute pain due to pulse takes place. The following very simplified summary
sensitization of receptors (free nerve terminals of C-fibers (see also Fig. 5.2) may be helpful in understand this process.
and Ali-fibers) to other chemical mediators making up the As mentioned earlier, the nociceptive impulse reaches the
"inflammatory soup" (Besson, 1999). In particular, because dorsal horn of the spinal cord through unmyelinated
prostaglandins are involved in the sensitization and acti­ C-fibers and thinly myelinated Ali-fibers, where they are
vation of free nerve terminals and prostaglandins are syn­ switched on to the second neuron (labeled "WDR neuron"
thesized by the enzyme cyc]ooxygenase (COX), COX inhib­ for 'wide dynamic range neuron' in Figure 5.2 as it receives
itors have become a frequent choice in treatment of acute afferent input from different fibers). In addition, C- and Ao­
pain. Prostaglandins also help to establish structural fibers give simultaneous, collateral impulses to GABA-ergic
changes in the synapses, thereby increasing transmission and opioidergic neurons of the spinal cord (Fig. 5.2). These
in the synapses of the central nervous system, particularly GABA-ergic and opioidergic neurons reduce the excitatory
in the dorsal horn of the spinal cord. influence on the WDR neuron by their action, and raise the
COX is therefore important for pain in the acute phase. stimulus threshold (i. e., the WDR neuron becomes inhib­
However, according to recent research, many mechanisms ited). At the same time, descending pathways from the
remain elusive. In chronic pain, i. e., when there is no midbrain also act on WDR, GABA-ergic and opioidergic
apparent tissue lesion or when an inflammatory reaction neurons via norepinephrinergic (NE) and serotoninergic
is not evident (for which rheumatoid arthritis may be an (5HT) pathways. These descending pathways then addi­
exception), COX may be of limited importance. Other tionally contribute to the inhibition of the WDR neuron.
grounds for chronic pain must accordingly be considered. The nociceptive impulses are modified due to these pro­
cesses, and pass up the spinal cord and through the thala­
mus to the cerebral cortex where they are perceived as
Gate- Control Theory pain.
Once nociceptive impulses enter the central nervous
In 1965 Melzack and Wall set a milestone in the under­ system (i. e., "gate open") this information is spread out
standing of the pain phenomenon with their gate-control to different parts including spinal cord, medulla, and cor­
theory (Melzack and Wall. 1965). This theory was the first tex. Reflex phenomena are triggered (e. g., on the level of
to integrate nociceptive impulses as well as emotional and the spinal cord) due to spreading of the nociceptive im­
cognitive aspects of pain experience. Gate-control theory pulses and endocrine reactions may follow (e. g., induced

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by the hypothalamus). In terms of triggering cognitive and


emotional activity, the same impulses are finally processed
in the brain cortex. Regarding descending modulation due
to NE and 5HT, it is important to note that these neuro­
transmitters are critically involved in psychologic function­
ing, in particular the regulation of the emotional and affec­
tive status of a person.
Conclusions of importance for a treatment strategy in
chronic pain that can be drawn from the processes involved
in the modulation of pain are: (a) Insufficient inhibitory
modulation of the centripetal nociceptive impulses is cen­
tral to the development of chronic pain; and (b) both
physiologic and psychologic influences exert an inhibitory
modulation on the nociceptive impulses by the appropriate Fig. 5.2 Gate-control theory: scheme of modulation of the noci­
pathways and are responsible for the development of ceptive impulses.

chronic pain.
The modulation of nociceptive impulses as outlined tioned above, nonnociceptive impulses may excite this
above is a restraining of the nociceptive impulse. Experi­ neuron and be perceived as pain; and (2) as a result of
mental investigations have shown that inhibitory modula­ biological changes, the WDR neuron shows an unusually
tion is insufficient with therapy-resistant and/or chronic high spontaneous discharge which, once again, is perceived
pain (Besson, 1999). Research has also demonstrated that as pain. These biological changes are also known as the
neurobiological changes of the WDR neuron may take place "wind-up" phenomenon and represent the basis of central
(Besson, 1999; Hoheisel et al.. 1994) because of inadequate sensitization (Besson, 1999; Dickenson, 1995). Considerable
inhibitory modulation of the nociceptive impulse. These importance is currently given to the process of central
changes may occur in a very short time and can briefly be sensitization in the development of chronic pain. Given
described as follows: The nociceptive impulses arise, for this central sensitization, and in particular the fact that
example, from an inflammation or a peripheral lesion in the biological changes of the WDR neuron that have been
which the chemical mediators in the so-called "inflamma­ described can take place rapidly (Hoheisel et aI., 1994), an
tory soup" play a role. These mediators generate the noci­ important aspect of pain treatment is the prevention or
ceptive impulses (C- and A8-fibers), thereby stimulating reversal of central sensitization.
the WDR neuron. The sustained nociceptive stimulation It is known that under some circumstances the WDR
of the WDR neuron (mainly by the glutamatergic C-fibers) neuron may change its biological properties either to fire at
results in a sustained depolarization (i. e., excitation) of this a higher rate or to fire under the influence of many other
neuron. In this case, the binding of glutamate in the afferent impulses. In this case even nonnociceptive im­
C-fibers on the WDR neuron's N-methyl-D-aspartate pulses may lead to pain (such as simple limb movement,
(NMDA) receptor is crucial. This receptor is responsible slight tissue pressure). This gives the impression of over­
for controlling calcium ion channels. Opening calcium ion sensitivity when pain results from mild (i. e.. usually non­
channels, among other actions, sets the second-messenger pain-inducing) stimuli, and may be seen as a psychologic
system in motion, followed by the transcription of the problem of the patient. Indeed this frequent clinical obser­
genetic information and increased gene expression (by vation is based on hypersensitivity of the central nervous
the so-called immediate early genes). This expression is system. Once hypersensitivity is established, treating pain
followed by increased reproduction of NMDA receptors with pharmacologic agents may only increase problems.
on the WDR neuron. This appears to be a biologically sig­
nificant mechanism that should protect the WDR neuron
from excessive stimulation. However, changes in biological Conclusions
characteristics of the WDR neuron can result from an in-
creased density of NMDA receptors on the neuron. This Given that chronic pain results from changes in biological
may have the following consequences: (1) since there is a properties of the WDR neuron, the principal issue will be to
higher density of NMDA receptors on the WDR neuron, act on modulation (i. e., downregulation of the impulse
many presynaptic impulses (which are often numerous) ratio). Careful consideration of the facts outlined above in
can contribute to the sustained depolarization of this neu­ treating chronic pain leads to the conclusion that prescrip­
ron. In relation to chronic pain, the most important con­ tion of prostaglandin synthesis inhibitors alone is of limited
sequence is that due to changes in the WDR neuron men- value. These chronic pain agents may have some influence

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on nociceptive impulses (e. g.. in rheumatoid arthritis cord. p-Endorphin is mainly found in the hypothalamic
where continuous tissue damage may take place). COX arcuate nucleus and the midbrain periaqueductal gray mat­
inhibitors may have an additional positive effect in reduc­ ter. Dynorphins have similar distribution to enkephalins
ing the rate of synaptic transmission in the central nervous (Fields. 1987).
system. which is under the influence of prostaglandins. It is To summarize: According to the distribution of opioid
more important to consider that treatment of chronic pain receptors and endogenous opioids. the main site of action
using only pharmacologic agents may fail because the doses of opioids is at spinal and supraspinal levels. Spinal and
required for complete analgesia may be greatly exceed the supraspinal mechanisms of opioid actions are synergistic.
level at which toxicity occurs. The treatment benefit for In addition. the fact that opioid receptors exist in the pe­
chronic pain while using NSAIDs is only very limited be­ riphery suggests that opioids are likely to act on structures
cause influence on downregulation of the WDR neuron outside of the central nervous system as well. Opioids
cannot be provided. This indicates that in chronic pain should be used for moderate or severe nociceptive pain.
the pharmacologic treatment will have to focus on different Their efficacy in neuropathic pain seems to be poorly sup­
pharmaceutical substances. and that other nonpharmaco­ ported by clinical routine.
logic strategies may be helpful. Given that in many chronic It is well established that there are genetic variants of
pain syndromes the downregulation of the WDR neuron is the receptor (Pasternak. 1999) and this variation is con­
required. NSAlDs may be employed rather than opioids. sidered responsible for differences in receptor affinity of
different opioids and contributes to their analgesic poten­
tial. It has been suggested. although not yet proven
Pharmacologic Treatment (McQuai. 1999). that side-effects of opioids (nausea. vomit­
of Chronic Pain ing. sedation. in some cases hallucinations) are connected
with the different receptor affinities of opioids.
Opioids These agents are categorized into the following groups
according to their affinity for opioid receptors: agonists.
In acute pain. particularly postoperative pain or other se­ partial agonists (e. g.. buprenorphine). agonists/antagonists
vere pain. or moderate to severe chronic pain opioids ap­ (e. g.. butorphanol. nalbupbine. pentazocine. and dezocine).
pear to be the drug of choice. This is clearly supported by and antagonists (naloxone. naltrexone. and cholecystoki­
extensive clinical experience. The choice of opioid. route of nin). Not all substances with opioid-receptor affinity ate
administration. and sometimes variation between the employed in treatment. mainly on the basis of cost­
drugs should be carefully considered. Opioids (from opium. effectiveness analysis in which the balance between effect
which is the Greek term for juice. i. e.. extract from the and side-effects is crucial. Most of the widely used opioids.
poppy plant) are a group of morphinelike substances as well as doses and additional comments. are summarized
with primarily analgesic properties. in Table 5.1.
The pharmacologic effects of all opioids are based on The main advantage of opioids in treatment of pain is
their interactions with the three opioid receptors mu (Il). their excellent and quick acting analgesia in moderate and
kappa ( K ) . and delta (8). which were discovered in the early severe pain. An experienced professional with the proper
1970s. The mu receptor is the principal structure in the equipment should administer opioid treatment. especially
analgesic action of opioids. Opioid receptors exist in the if the parenteral route of administration is preferred.
periphery. in the spinal dorsal horn. in the brainstem. in the There is usually no ceiling effect with opioids (increased
thalamus. and in the cortex. The main effects of opioids dosage provides increased analgesia). Opioids are available
include a decrease of presynaptic transmitter release. hy­ in different forms and can be given by oral. sublingual.
perpolarization of postsynaptic neurons. and disinhibition. parenteral. rectal. intraspinal. or transdermal:
The discovery of opioid receptors encouraged the search enteral administration (preferably intravenous. providing
for endogenous substances that might be responsible for the possibility for better titration) should undertaken in
modulation of action. This research identified enkephalins. severe acute pain. In chronic pain. parenteral administra­
endorphins. and dynorphins. In the 1980s precursor mol­ tion of opioids should give way to preferred long-acting
ecules of endogenous opioid-receptor agonists were iden­ opioid forms. Morphine is still the standard and the belief
tified: preenkephalin. proadrenocorticotropic hormone that other drugs act faster or longer or possible have fewer
(pro-ACTH). ACTH endorphin (propiomelanocortin). and side-effects is unsupported by clinical evidence (McQuai.
prodynorphin. The localization of the endogenous opioids 1999). The choice of opioid. the matter of tolerance. pain
was identified. Enkephalin is found in the amygdala. hypo­ sensitivity to opioids. and the decision to switch one opioid
thalamus. the midbrain periaqueductal gray matter. the for another. or to change the mode of administration. re­
rostroventral medula and the dorsal horn of the spinal main matters of contention (McQuai. 1999).

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Table 5.1 Opioids in chronic pain treatment

Recommend­ Comment
ed Average
24 ho ur
-

b
Dosage

Opioids for mild to moderate pain

Codeine 15-50 mg 200mg 4-6 h Short-acting. weak analgesic

Dextropro- 65 mg 150-300 mg 8-12 h


poxyphene

Dihydroco- 60-120 mg 120-240 mg 3-4 h (12 h) Controlled in some countries: release form available with
d e ine 12 h dosing interval

Tilidin 50-100 mg 200-300 mg 2-3 h Controlled in some countries: release form available with
(8-12h) recommended 8-12 h dosing interval

Tramadol 50-100 mg up to 2-4 h Different forms available in some countries (oral.


400-600 mg (8-12 h) subcutaneous. intravenous. rectal. and controlled-
release). Easily prescribed in some countries due to lack
of particular prescription regulations. Potent sedation.
Frequent nausea/vomiting

Oploids for moderate to severe pain

Buprenorphine 0.2-0.4 mg ? 6-8 h Doses over 4 mg do not show higher analgesia

Fentanyl SO-lOOl1g 0.5-1 h Quick onset of action. short half-life. Very potent
analgesic. Respiratory depression may not be obvious
for minutes. Several application forms. High comfort
with transdermal application form in different doses
with 72 h analgesic action. Considerable side-effects in
some patients (e. g .• nausea/vomiting)

Hydromor- l.Smg 3-4 h Quick-action onset with a short half-life. Very potent
phone (oral 7.5 mg) analgesic. Several application forms

Levophanol 2mg 6-8 h High analgesic potential. Careful dose titration. May
(oral 4 mg) accumulate considerably

Meperidine 100mg 300mg 2-3 h Toxic metabolite that may provoke seizures
(8-12 h)

Methadone 10 mg 30-40mg 6-8 h Short analgesic action. long half-life. May accumulate
(oral 20 mg) with dose increase to cause toxic effect

Morphine 10 mg 3-4 h Standard opioid. In many respects the "gold standard"


(oral 30 mg) to which analgesic effect of other opioids is compared in
terms of equianalgesic potential. Several application
forms include controlled release with long- term action

Pethidine SOmg Recommend- 3-4 h Several application forms. Active metabolite Norpethi-
(oral 150 mg) ed max. dine is potentially toxic. First- pass effect is significant.
SOOmg Caution in hepatic failure

Propoxyphene 3-6 h Not recommended for routine administration. Toxic


metabolite

·Considerable differences in the recommended average single dose should be conSidered in drugs with different application forms where, for
example. intravenous, subcutane ous, or intramuscular doses are usually significantly lower then oral doses.

bOpioids have no ceiling effect. For this reason the recommended average 24·hour dosage should be taken as a guideline only.
Some opioids in the table are not available in every country. Drugs exist in different application forms (e. g., for intravenous. rectal, or transdermal
use, or in controlled-release form) not all of which are available in all countries. All countries have their own specific restrictions for opioid prescription
that need to be followed. Furthermore, in every individual patient. general prescribing aspects side-effects and adverse effects and development of
tolerance and dependence should be taken into consideration and related to the patient's disposition.
It is strongly recommended that opioid treatments, in particular those with high analgesic potential. be restricted to experienced professionals. This
is particularly so for initial opioid treatment. No opioid analgesics should be taken in combination with monoamine oxidase inhibitors (MAOI) due to
possibly dangerous side-effects (e. g., respiratory depreSSion, hypertension) some of which may be fatal.

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It is known that in some patients the therapeutic po­ istration. or 90 minutes of subcutaneous administration.
tential of a given opioid may diminish over time. In such Respiratory depression is a very dangerous side-effect due
cases a change from one opioid to another (so-called rota­ to the subsequent depression of the central nervous
tion) may be necessary. This is usually done as follows: first system; it can be predicted using other symptoms such
the equivalent dose to that of the replaced opioid should be as drowsiness. mental clouding. or severe sedation. Some
found using existing equivalency tables. Equivalencies are opioids (e. g.. meperidine) can cause excitation or seizures.
based on intramuscular morphine doses in opioid-naive possibly as a consequence of its metabolite normeperi­
individuals. which may differ considerably in patients dine. Other relatively frequent side-effects at higher doses
treated with opioids over a long period. For this reason. include myoclonus or clonic spasm of a single muscle or a
the treatment should be started with 50% of the equivalent group of muscles. Emetic side-effects. causing nausea or
dosage and the dosage of the new opioid increased step by vomiting. usually occur in the initial phase of treatment
step according to analgesic effect and side-effects. How­ and tolerance is obsetved in most patients (McQuai. 1999).
ever. improvement of the analgesic effect has been shown Nausea and vomiting are caused by chemoreceptor trigger
to be possible by change in the route of administration. zone stimulation. They can be managed by antiemetics but
making rotation unnecessary (Kalso et al.. 1996). and this there are a few cases with unmanageable nausea or
should also be considered. vomiting that could require a change to another opioid
or even the discontinuation of opioids altogether.
The proportion of patients showing tolerance and de­
Side- Effects of Opioids
pendence following prolonged use of opioids is not known
The main side-effects are seen in central nervous system exactly for various reasons. Clinical experience suggests
activity (euphoria or suppression/inhibition of different that tolerance to opioids develops more rapidly with a
kinds) as well as nausea. vomiting. and constipation. These parenteral route of administration. in particular with
can be understood from the fact that the same opioid drugs with short half-life. In addition. favorable psycho­
receptors mediate both analgesia and physiologic phe­ logic effects may be responsible for development of
nomena. Active metabolites may also contribute to these tolerance and the requirement for higher doses. Patients
adverse effects (e. g .. norpethidine causing tremor or con­ who develop tolerance usually complain of decreased du­
vulsions; normeperidine with its seizure potential; or the ration of analgesic effects. Clinical experience shows that
possible toxicity of morphine-6-glucuronide. particularly drug-seeking behavior does not occur in patients whose
in patients with impaired renal function). Compared on relief of pain is achieved by the use of opioids (Porter and
the basis of the same degree of analgesia. adverse effects Jick. 1980). Abrupt discontinuation of opioids introduces
do not seem to differ between opioids (McQuai. 1999). withdrawal syndromes including agitation. anxiety. in­
Constipation. a side-effect of all opioids. is based on cen­ somnia. tremor. tachycardia. muscle cramps. yawning.
tral and peripheral receptor affinity. Tolerance to the con­ lacrimation. fever. and signs of hyperexcitability of the
stipatory effects of opioids has not so far been confirmed. sympathetic nervous system. Opioid-insensitive pain.
calling for adequate treatment for affected patients (e. g.. although infrequent. may still occur in cancer patients
stool softeners or laxatives). Patients are also known to and as non-cancer-related pain (usually nerve compres­
experience problems in the urinary system (bladder sion or nerve destruction).
spasm. urinary retention. or urgency). Muscular problems
including spasms may cause agitation or anxiety. Fre­
quently the introduction of opioids in the treatment of COX Inhibitors; NSAIDs
chronic pain is compromised by the beliefs that these
drugs cause respiratory depression and frequently and Prostaglandin synthesis inhibitors (i. e.. inhibitors of cyclo­
unavoidably lead to tolerance and dependence. However. oxygenase) play a key role in the treatment of acute pain
it is suggested that nociceptive input in the respiratory given that prostaglandins are critically involved in the
center counterbalances the respiratory depressant poten­ generation of nociceptive impulses. Many of these substan­
tial (Borgbjerg. 1996). indicating that patients suffering ces show excellent analgesic effect in mild to moderate
from severe pain may be at lower risk of respiratory pain as well as to some extent in acute pain. In such cases
depression. Carefully titrated. appropriately sized. and NSAIR drugs show a similar analgesic potential to weak
well-timed doses of opioids can prevent respiratory de­ opioids. The use of NSAIDs is not followed by development
pression (McQuai. 1999). Observation is recommended of tolerance and subsequent dependence. These substan­
while using fentanyl intravenously. If at all. respiratory ces are easily available and inexpensive (as in the case of
depression usually occurs within 10 minutes of intrave­ nonselective COX inhibitors). However. their specific an­
nous administration. 30 minutes of intramuscular admin­ algesic effect. especially in nonrheumatoid pain. is fre­

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NSAIDs
Activated by physiologic stimuli Activated by inflammation stimuli

COX-l COX-2
Constitutional enzyme Inducible enzyme

Target tissue Macrophages, synoviocytes

1 1
Thromboxane Proteases
(thrombocytes)

Prostacyclin Prostaglandins
(endothelium.
gastric mucosae)

Prostaglandin E2 Mediators of
(kidney) inflammation

! 1
Physiological functions Inflammatory reaction/pain

Fig.s.3 Regulation of prostaglandin synthesis by COX-1 and COX-2 (according to Vane, 1994).

quently poorly documented as studies with NSAIR have resulting from inflammatory process are essential in gen­
mainly been conducted with patients suffering from rheu­ erating pain, COX-2 inhibitors showed fewer of the side­
matoid arthritis. Parameters other than pain (e.g., inflam­ effects frequently observed with classical NSAlDs, i. e.,
mation of joints) were the main measures in these studies. upper gastrointestinal tract effects (Bombardier et aI.,
It is well known that the anti-inflammatory action and 2000; Silverstein et aI., 2000) or bleeding (FitzGerald and
analgesic effects do not remain in a linear relationship Patrono, 2001). COX-2 inhibitors were also introduced into
(McCormack and Brune. 1991). This makes it difficult to treatment of other pain conditions because of their anti­
understand the analgesic effect of NSAlDs mainly on the inflammatory action. Selective inhibition of prostaglandin­
basis of inhibition of prostaglandin synthesis. Prescription synthesizing COX-2 may provide important advantages in
of NSAlDs in chronic severe pain, which might be thought the treatment of pain, whereas possible side-effects result­
useful from the introductory material to this chapter, is ing from COX-1-inhibition may be prevented. However,
likely to need careful reassessment. There are studies in­ selective COX-2 inhibitors (i. e., inhibitors of prostaglandin
dicating that the analgesic affect of NSAIDs may result synthesis) did not show a superior analgesic effect when
from action in the central nervous system (Fabbri et aI., compared with nonselective COX inhibitors (Mazario et aI.,
1992). 2001) and therefore did not fulfill the expectations of them.
COX appears to have at least two isoforms (COX-1 and Recent views suggest that selective COX-2 inhibitors are
COX-2) between which there are important differences in less analgesic then nonselective COX inhibitors (FitzGerald
biological properties (see Fig. 5.3). COX-1 primarily acti­ and Patrono, 2001; Mazario et aI., 2001; Bensen et aI.,
vates physiologic functions in different tissues, whereas 1999). The role of selective COX-2 inhibitors in pain may
COX-2 is responsible for inflammatory reactions. Adverse be further complicated by the fact that acetaminophen, a
effects of traditional nonsteroidal anti-inflammatory drugs potent analgesic drug, has negligible inhibitory properties
(NSAlDs) and salicylates inhibiting both COX-1 and COX-2 on COX-lor COX-2. In addition, the previously assumed
are related to their inhibition of COX-1, which among its long-term safety of COX-2 is becoming increasingly ques­
other physiologic functions synthesizes gastroprotective tionable (I<aplan-Machlis and I<lostermeyer, 1999; Spiegel
substances (Bombardier et aI., 2000; Silverstein et aI., et aI., 2003). One of the COX-2 inhibitors (rofecoxib) has
2000). The anti-inflammatory and analgesic effects of been removed from the market (BMJ 2004; 329; 816).
NSAlDs were accordingly attributed to the inhibition of While the deliberations by the US Food and Drug Admin­
COX-2-dependent pathways. This led to the development istration (FDA) resulted in the decision that other COX-2
of COX-2 inhibitors, which were then introduced into treat­ inhibitors (celecoxib and valdecoxib) also carry serious
ment of rheumatoid arthritis. Apart from anti-inflamma­ risks of heart attack and stroke, the panel did not recom­
tory action and the assumption that chemical mediators

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mend that these drugs bei withdrawn from the market Considering the recent critical reviews of the develop­
(Lenze.2005). ment of improved pain-relieving drugs and the biological
COX-3. a variant of COX-1. has recently been identified basis of chronic pain discussed earlier in this chapter. the
as an inducible isoenzyme in later stages of inflammation prescription ofNSAIDs in patients with chronic pain (due to
(Willoughby et al.. 2000). Interestingly acetaminophen, a obvious reasons apart from rheumatoid arthritis) should be
substance with analgesic effect, has some of activity to questioned seriously (Scholz and Woolf. 2002; Curatolo
block the COX-3-variant. which gives rise to speculation and Bogduk, 2001).
that this COX-variant is significantly involved in pain. In Some commonly used NSAlDs are summarized in Table
addition, nonselective COX inhibitors (e. g.. diclofenac. ibu­ 5.2, which also contains some recommendations for doses
profen) show powerful COX-3 inhibition. indicating that and comments with regard to more substance-specific
inhibition of this COX-variant is important in the treatment side-effects.
of pain. It is interesting also that this COX-variant occurs The most prominent disadvantage of NSAlDs is their
not only in tissue but also in the brain and the spinal cord toxicity. predominantly in terms of long-term gastrointes­
(Chandrasekharan. 2002). This may raise doubt about the tinal intolerance and ulceration. However. this is mainly
explanation of the analgesic effect of nonselective COX observed during unusual chronic prescription over months.
inhibitors or acetaminophen. Because of the physiological action of COX. its inhibition by
NSAlDs are rapidly absorbed and are highly protein­ NSAlDs also compromises renal flow and has related con­
bound and have a low tissue distribution. NSAlDs are me­ sequences. These drugs do not show higher analgesic po­
tabolized in the liver with low clearance (Denson and Katz. tential with increaSing doses (i. e.. they show ceiling effects).
1992). It is important to acknowledge that salicylates com­ and their full efficacy usually occurs after several days.
pete with other NSAlDs for protein binding sites and may Furthermore. NSAlDs are usually not helpful in severe pain.
increase the concentration of some of these drugs to toxic It is important to reiterate that in contrast to acute pain,
level. Toxicity of NSAIDs is poorly documented as most where chemical mediators play an important role. these
studies have been conducted with elderly patients. Because substances are not evidently involved in chronic pain. Pre­
of the influence on physiologic processes in the organism. scription ofNSAlDs in chronic pain stages is poorly justified
with chronic prescription of NSAlDs a laboratory-con­ by the evidence base. The lack of therapeutic efficacy might
trolled examination of physiological parameters. with em­ frustrate the patient and only contribute to additional
phasis on renal function. should be performed periodically. problems in treatment.

Table 5.2 Nonopioid analgesics in chronic pain treatment

Comments

Overdose leads to hepatotoxicity. Careful


administration is needed in cases of
chronic alcoholism
.JI 'L__
Ii --.r--
Sallcylates
= -

Acetylated Aspirin 500-1000 mg 4000 mg 4- 6 h Inhibition of platelet aggregation. Com-


petes in protein binding with NSAIDs.
causing a potential toxic effect. Gastro-
intestinal bleeding and ulceration

Nonacetylated Diflunisal 1000 mg 1500 mg 12 h Gastrointestinal intolerance and bleeding


(less than aspirin)

Salsalate 1500 mg 2000-3000 mg 8-12 h Common side-effects of NSAIDs may


occur
=
Salsalate 1500 mg 2000-3000 mg 8-12 h Common side-effects of NSAIDs may
occur

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Table 5.2 Nonopioid a na lges ics in chronic pain treatment (co ntinued)

Average Comments
Single Dose

Propionic acid Ibuprofen 400-600 mg 2400 mg 4-6h Common side-effects of NSAIDs may
derlvates occur. Better tolerated than aspirin, with
fewer gastrointestinal side-effects. Low
incidence of hepatotoxicity

Arylacetlc acid Naproxen 250-500mg 1250 mg Common side-effects of NSAIDs may


derlvates occur. Long-term safety unknown

Fenoprofen 200mg 800mg 4-6h Common side-effects of NSAIDs may


occur

Ketoprofen 50-75mg 300mg 6-8h Common side-effects of NSAIDs may


occur

Phenylalka- Flurbiprofen 100mg 200mg 6-8 h Common side-effects of NSAIDs may


nold acid occur
derivates

Acetic acid Indometa- 25-50 mg 100-200 mg 6-12h Gastric mucosal inflammation, or necrosis
derlvates cin with bleeding. Careful administration in
positive history of gastric bleeding. Irri-
tation possible in some patients

pyranocarbox- Etodolac 300-600 mg 600-1200 mg


yllc acid deri-
vates

Tolmetin 200-6oomg 1800 mg 6-8h High gastrointestinal toxicity may occur

Indene Sulindac 150-200 mg 400mg 12h Common side-effects of NSAIDs may


derivates occur

Diclofenac 50-75mg 200mg 68h Good analgesic, usually well tolerated.


Frequently considered as a first-choice
NSAID

Anthranilic
acid derlvates

Fenamate Mefenacid 500mg 500-1500 mg 6-8h May cause upper gastrointestinal prob-
lems. Shows good analgesia if tolerated

Keto- enol acid


derlvates

Oxicams Piroxicam 20mg 20-40 mg 24h Monitoring of renal parameters recom-


mended in cases with longer administra-
tion

Tenoxicam 20mg 20-40mg 12- Upper gastrointestinal tract side-effects


24h may be frequent, leading to intolerance
and compliance problems

Meloxicam 7.5mg 7.5-15 mg 12- Must be avoided in hepatic failure. Careful


24h control of renal parameters is recom-
mended

Pirazolldlne- Phenylbuta- 200mg 200-60mg 12h GastrOintestinal, renal side-effects or


dlones zone bronchial spasms may be frequent

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Table 5.2 N onop io i d analgesics in chronic pain treatment (con ti nu ed)

Recommend­ Comments
ed 24-nour
Dose

Other derivates

Nimesulid 200mg 400mg 12 n Snould not be taken by patients with


positive history of gastrointestinal
bleeding or renal failure

Pyrazollnones Pnenazone 200mg 600-800mg 4-6h Must be avoided in hepatic or renal


failure. May cause allergy

Propypne­ 250mg 500-750 mg 4-6 n Contraindicated in a number of


nazone gastrointestinal problems including
porphyria (list of disorders indicating
restriction in use should be taken into
account On an individual basis)

Metamizole 500-1000mg 4000 mg 4-6 n May cause thrombocytopenia, leuko­


penia or agranulocytosis

Pyrldyl carbamate Flupirtin 100mg 300mg 6-8h

Coxlbs Rofecoxib 12.5-25mg 25-50mg Once Different doses for acute or chronic
(COX-2 inhibitors) daily pain are recommended. Advantages
depend mainly On selectivity or lack of
inhibition of COX- 1 (e. g., gastroin­
testinal or renal side -effects)

Celecoxib 100mg 100-200mg Once May have Significant interactions due


daily to blockage of different lines of the
cytochrome- P-450- enzymes. Precise
information of all medications used by
the patient is necessary. Advantages
of COX-2-inhibitors. Clinical experi­
ence may indicate lower analgesic
effect.

Valdecoxib 10-40mg Side-effects seen in other coxibs may


occur. Caution in renal or hepatic
failure

Note: Table 5.2 contains the routinely used nonopioid analgesics. frequently referred to as nonsteroida l anti·inflammatory drugs (NSAIDs). Some are
not available in certain countries. In addition. some of these drugs do not belong to the group of NSAIDs in the strict sense. Not every probable side­
effect or toxic effect can be considered. Most possible side-effects can be better u n derstood if the NSAID mechan i s m of action is also understood
(see also Fig. 5.1 for the b i osynthesis of eicosanoid s ). Before treatment is given to patients with a history of adverse effects or presumed risk for
adverse effects (in p a rticular gastrointestinal or renal problems or asthma). careful choices of the drug and frequent clinical and laboratory
monitoring are imperative. Particular care in the use of NSAIDs is recommended in early pregnancy (it is recommended that many of these drugs are
avoided. with the possible exception of acetaminophen). With all NSAIDs monitoring of gastrointestinal. vascular. blood. and renal parameters is
particularly important in chronic use. Coxibs are frequently considered to show few gastrointestinal side-effects. Newer research may support the
view that coxibs have advantages mainly in patients with a history of gastrointestinal bleeding. Many substances in this table may cause allergic
reactions.

Acetaminophen and metamizol have numerous advan­ usually well tolerated with few toxic or other side-effects;
tages: they show no adverse effects on gastrointestinal these are often exaggerated and poorly supported by
tract mucosa, on kidney, or on platelet aggregation. How­ clinical routine. Possible adverse effects are mentioned in
ever, they may have an analgesic effect in cases with mild Table 5.2.
and sometimes moderate pain chronic pain. Both drugs are

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Other Pharmacologic Interventions larger clinical studies such as pregabalin) show consider­
able advantages in treating neuropathic syndromes
In adjuvant treatment, a heterogeneous group of pharma­ (Sindrup and Jensen, 1999). Gabapentin is usually well
ceuticals, based on clinical observation, play a role believed tolerated with few side-effects, such as limited-duration
to show some beneficial effect in the treatment of chronic headache and dizziness, and has high efficacy in neuro­
pain. However, recent reviews seriously question the em­ pathic pain. However, the maximum effect requires suffi­
pirical basis of employing these different pharmaceuticals cient doses (e. g., above 1600 mg/day: most patients re­
in the treatment of chronic pain (Curatolo and Bogduk, quire doses of 2400-3600 mg/day): in clinical routine this
2001). However, adjuvant pharmacologic treatment seems is unfortunately frequently neglected, and syndromes that
to show considerable advantages especially when taken in are difficult to treat continue. Clinical observations indicate
combination with other pain-relieving substances. that a combination with tricyclics (effective in diabetic
Most attention in adjuvant treatment of pain has been neuropathy), codeine, and newly developed anticonvul­
placed on antidepressants. The introduction of antidepres­ sants such as gabapentin may show more benefit. Admin­
sants in pain treatment is based on the association of istration of antidepressants, anticonvulsants, and local
descending pathways (i. e., noradrenergic and serotoner­ anesthetics is supported against neuropathic pain (McQuai,
gic) in the modulation of nociceptive impulses. Since these 1999).
neurotransmitter pathways are inherently involved in the In systematic reviews, only muscle relaxants or muscle
regulation of patients' emotional status, their involvement relaxants in combination were identified as an effective
could be of particular importance in patients who, in treatment of pain associated with muscle spasm (Aker et
addition to pain, suffer from affective symptoms. Biolog­ aI., 1996). However, their effect seems to be better sup­
ically, these symptoms may indicate a comparative insuf­ ported in acute rather than in chronic musculoskeletal pain
ficiency of descending modulatory neurotransmitter path­ (Van Tulder, 1997). Baclofen has recently been shown to be
ways (i. e., serotonin and norepinephrine). However, a effective using specific indications such as neuropathic
systematic review did not confirm benefits in treating pain associated with dystonia (von Hilten, 2000).
chronic low back pain with these agents (Turner and Corticosteroids are a further group of substances with
Denny, 1993). Nevertheless, the antidepressants, in partic­ analgesic effect, usually in combination with other potent
ular tricyclic agents (e.g., amitriptyline, usually in doses analgesics, and may be used for quite specific indications.
lower than those used for treating clinical depression) are These indications may include bone metastases, spinal cord
considered important adjuvant agents in the treatment of compression, acute nerve compression, and increased in­
chronic pain (Watson, 1994). It is believed that these tracranial pressure. Corticosteroids may further be indi­
agents may lead to the relief of pain while showing an cated with epidural injections in disk herniation pain, spi­
improvement in mood, reduction in the level of potential nal stenosis, or foraminal stenosis, both lumbar or cervical
depression, and promotion of sleep. It is important to add (Curatolo and Bogduk, 2001).
that sleep is Frequently disturbed in chronic pain patients In recent years antidepressants and neuroleptics were
and sleep deprivation may contribute to this vicious cycle. frequently introduced into the treatment of chronic pain.
It is also proposed that tricyclic antidepressants may have Usually a combination of haloperidol and tricyclic antide­
a direct effect on nociceptive afferents (e. g., by blocking pressants (e.g., amitriptyline) was used. This is no longer a
sodium ion channels) and that they are particularly effec­ standard in the treatment of pain syndromes. Currently
tive due to the augmentation of analgesic response to neuroleptics or benzodiazepines are rarely introduced in
opioids. the treatment of pain syndromes. Sometimes in severe
Specific treatment may be required for neuropathic pain cancer pain, neuroleptics (e.g., haloperidol in individually
syndromes (postherpetic, diabetic, or due to damage of a titrated doses between 1 and 10 mg or more) may be
plexus, nerve root, or single nerves). NSAIDs are usually required to help relieve patients. Lately, neuroleptics are
ineffective in neuropathic pain, with even opioids not al­ being used as a single substance in combination with
ways showing sufficient analgesia. On the basis of the highly potent opioids. Benzodiazepines (e.g., alprazolam)
underlying mechanism of pain in neuropathic syndromes, may be prescribed on a carefully timed, limited schedule in
which have been treated using classical anticonvulsants patients who suffer from anxiety in combination with their
(e.g., phenytoin, carbamazepine, clonazepam, gabapentin), pain.
these agents are considered important in treating neuro­
pathic pain (e.g., following surgical treatment or posther­
petic, poststroke, or trigeminal pain or in diabetic neuro­
pathy). Newly developed anticonvulsants (e.g., gabapentin
or the even more recently developed substance entering

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known as transduction. The action potential ascends to the


Psychologic Aspects of Pain Treatment cortex (transmission). In this process the signal. or electri­
cal impulse, first reaches the dorsal horn of the spinal cord.
According to the International Association for the Study of At this site the afferent nerve synapses with the neuron of
Pain (IASP). pain is "an unpleasant sensory and emotional the spinothalamic tract below the WDR neuron. The signal
experience associated with actual and potential tissue continues to travel to the thalamus along the spinothalamic
damage. and is described in terms of such damage" (IASP. tract and from there to various areas of the cortex. Pain is
1979). This definition includes the psychologic aspect in perceived as soon as the signal reaches the cortex (percep­
both acute and chronic pain. but in clinical routine the tion). The nociceptive signal is modulated under the influ­
investigation of a pain patient requires first the search for ence of different structures in different levels of the central
a possible organic cause. Although pain is frequently con­ nervous system. Depending on the process of modulation
sidered as an exclusively nociceptive phenomenon (Turk in particular. subjects will experience pain in different ways
and Okifuji. 1999). individual differences in pain reporting, and show various somatic, psychosocial. and functional
following the same potentially pain-provoking procedure; manifestations. These phenomena will influence behavior.
impressively indicate that nociception is not always asso­ i. e., how people react to (e.g.. avoidance. withdrawal) and
ciated with pain experience. In contrast. pain experience in communicate (e.g.. shouting. crying) experiences of pain
the absence of nociception is a well-acknowledged phe­ and related distress. Finally, pain may cause suffering,
nomenon. Indeed, pain is a perceptual phenomenon in­ mainly resulting in the loss of aspects inherently connected
volving different eNS mechanisms for which nociception with the individual (understood in terms of being indivi­
may be a requirement. If an organic cause for pain is not sible and unique) such as functional ability, social status, or
found. an underlying psychologic cause is usually assumed social role. Suffering is indeed a psychologic or inherently
and the patient is referred to psychologic or psychiatric emotional reaction to pain and may explain why people
treatment. The introduction of a psychologic dimension suffering from pain display exaggerated behavior (fatigue.
in the experience of pain by the IASP definition shows exhaustion. lack of concentration. etc.).
that pain cannot be evaluated or treated irrespective of a The important aspect of psychologic intervention
person's disposition. To understand a person's disposition should focus on suffering. Initially an improvement of emo­
and to incorporate these aspects into the treatment. one tional status using medication should be sought. followed
must consider their past and current situations. Different by the search for strategies for the compensation of the loss
aspects of the patient's past. in particular circumstances experienced: alternative functions. supportive activities,
under which the emotional development occurred. are possibly providing acknowledgment in the social environ­
very important. Personality factors (i. e.. traits) established ment, helping to identify new roles and gathering positive
on the basis of how a person copes with different difficul­ experiences; all of these with gain of emotional status in
ties are also important (Engel. 1959; Blumer and Heilbronn, mind. Ultimately, in patients in whom pain cannot be suf­
1982). Assessing these may increase understanding of cur­ ficiently influenced. the improvement of quality of life may
rent psychosocial dispositions (e. g., marital and family sit­ become the main focus of psychologic therapeutic inter­
uation, job-related factors). These very specific aspects of vention.
pain experience may require the involvement of an ex­ Initially. the assessment of the patient's emotional sta­
perienced psychotherapist, particularly during treatment. tus is necessary. A number of chronic pain patients suffer
Recent studies clearly indicate that cognitive aspects may from the conditions discussed above and will develop so­
play the most important role in pain (Pincus and Morley, called emotional or affective disturbances. There are many
2001). The focusing of attention also appears to be of studies indicating patients suffering from chronic pain
particular relevance (Petrovic and Ingvar. 2002) and dis­ without demonstrating symptoms of clinical depression
traction of attention is one of the most important psycho­ (Novy et ai., 1995; Williams and Richardson. 1993; Rada­
logic interventions in the cognitive behavioral treatment of nov et ai., 1996). However, these symptoms may be sum­
pain. Although distracting attention from-pain related fac­ marized as a chronic form of adjustment disorder with
tors can be helpful in acute pain conditions. it may become mixed emotions according to DSM-IV (American Psychi­
difficult in chronic pain for which continuous attention atric Association. 1994). This means that the most prom­
distraction is required. inent symptoms are dysphoria, irritability. anger, and sad­
The following brief summary outlines the psychologic ness; it is important to treat these symptoms since affec­
and behavioral aspects of pain and the need to integrate tive nonequilibrium may lead to vegetative symptoms
these into a treatment strategy. The nociceptive process such as somatic hypelvigilance. sleep disturbances (non­
starts where tissue damage occurs. causing the generation restorative sleep), poor concentration. and reduced libido.
of an initial stimulus in the afferent nerve fibers; a process Many of these symptoms can eventually lead to a vicious

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cycle with a nontreatable chronic disorder. For this reason ment has been comprehensively summarized (Turk and
the first step at this stage might be pharmacologic treat­ Meichenbaum, 1994) and will therefore be dealt with in
ment of the affective problem. Antidepressants may brief . Cognitive behavioral therapy focuses on disruption of
chiefly be required. The choice and doses of drug should, the vicious cycle generally outlined above. An initial re­
however, be carefully considered in order to avoid side­ quirement is for the patient to learn that pain is manage­
effects in patients with frequent suffering from severe able to the point that at least some improvement of quality
forms of somatic hypervigilance. Tricyclics may show anti­ of life is possible. This is a main goal of treatment rather
cholinergic effects and selective SSRI may cause gastro­ than focusing on total pain relief . The following techniques
intestinal problems in men who, due to pain. may suffer are used in this treatment.
significant libido loss and, due to further action on post­ Education is a fundamental part of the treatment. The
synaptic terminals, additional sexual problems. Given that patient should know the essentials of pain such as how it is
clinical depression is not seen in the greater part of these generated and modified and what might improve the mod­
patients, lower doses of antidepressants may be the treat­ ification of this pain. In particular, patients should know
ment of choice. Substances that positively influence sleep about the factors or activities that might may aggravate as
(e. g., amitriptyline, trimipramine) may be the best choice well as alleviate the pain. This may enable the patient to
to start with, particularly as an initial positive effect may analyze his or her own behavior, uncover which activities
strengthen therapeutic aUiance and profound Iy influence might aggravate or alleviate the pain, and foster positive
the course of treatment. aspects crucial to developing further activities and helping
break out from isolation. Additional positive effects of this
may include increased participation in physical activities
Cognitive Behavioral Therapy that do not provoke pain, a gain of physical fitness, social
reintegration, and development of distractors.
Apart from treatment with antidepressants. and where Distraction is a refocusing of attention away from the
necessary with other drugs, modern psychologic therapy pain experience (McCaffery and Beebe, 1989). The most
of chronic pain is mainly based on cognitive behavioral favorable distractors are those that are enjoyed by the
therapy. The basis of this therapy that pain is not simply patient and therefore add to the affective benefit. One
a sensory event but that experience of pain also includes should avoid giving patients suggestions or prescriptions
affective, cognitive, and behavioral aspects. The main as­ of what to do in order to distract. In this regard, an analysis
pects of cognitive behavioral therapy are to enable the of behavior under close observation of the therapist is
patient to control this pain and alleviate consequences crucial. This should include the analysis of aggravating
previously summarized under what is referred to as suffer­ activities (to be avoided if possible) or those alleviating
ing. The achievement of these goals may significantly im­ symptoms (to be fostered). This is the best way to find
prove the quality of life. The therapy is based on the expe­ individual distractors, with a preference for those with
rience of chronic pain patients who had the increasing positively affective reactions. These should be pleasurable
belief that they had done everything to control the pain activities or stimuli that correspond to particular situations
without success and were consequently afraid of the pos­ The patient should engage in finding these activities and, in
sibly serious underlying cause of pain and its degeneration. the case of positive effects, should be encouraged to per­
In many patients this leads to the reduction of both phys­ severe in them.
ical and social activities in the belief that these may be Relaxation techniques are increasingly being employed
painful or may cause an increase the pain. In these cases in cognitive behavioral treatment. Relaxation may help to
the onset of vita minima (minimal life activity) is a frequent reduce fear and anxiety, thereby introducing additional
consequence that enhances suffering. This inevitably leads positive feelings. Many pain patients show increased levels
to an increased loss of muscle strength and joint mobility, of negative affects (such as anxiety and fear). leading to
and a continuous decrease in fitness. Many of these pa­ increased activity of the autonomous nervous system with
tients develop a defeatist attitude and rely on the hope that potentially pain-provoking consequences. Indeed, many
by a "miracle" their pain might vanish. At this stage, pa­ patients under sustained stress show increased muscle
tients focus on themselves in fearful expectation without tension, an important aspect of pain promotion. Techniques
distractors or positive experiences. In terms of cognitive of autogenic relaxation training, progressive muscle
behavioral psychology, these individuals show dysfunc­ relaxation, imagery, biofeedback (e. g.. muscular, respira­
tional behavior in which pain controls the patient rather tory), or hypnosis can prove useful. Many of these tech­
than vice versa (Pincus and Morley, 2001). niques, in particular imagery and biofeedback, should be
Cognitive behavioral treatment is the standard thera­ performed under the assistance and supervision of an
peutic measure for chronic as well as acute pain. This treat- experienced therapist; working on different aspects of

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The Phannacologlc and Psychologic Treatment of Chronic Pain

emotional experience may be essential for a change of Family involvement or systemic intervention in the
behavior. Some authors suggest music therapy as an addi­ treatment of chronic pain is also very important. Pain af­
tional aspect of cognitive behavioral treatment. It is be­ fects family life in many ways, as it affects the social role of
lieved that music relaxes and has similar effects to other the patient. Although there is limited research on this
relaxation techniques. aspect, personal experience supports this type of interven­
tion.

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6 Nonradicular Pain:
Spondylogenic and Myofascial Pain Syndromes

Prior to the landmark article by Mixter and Barr (1934), spective, this is understandable (Dvorak, 1982b, 1983;
who described the characteristics of sciatica following disk Gibson, 1980; Wardwell, 1980). The scholarly work and
herniation with subsequent surgical correction, legion pa­ scientific language used by such pioneering investigators
pers were published attempting to explain the different as Korr (1975) and Wyke and his colleagues (1967, 1979b)
musculoskeletal pain syndromes, often on the basis of have fundamentally contributed to a better understanding
empirical descriptions and hypothetical postulates. Partic­ of some of the neurophysiologic principles underlying
ular interest in the source of pain originating from soft­ musculoskeletal pain phenomena.
tissue structures such as muscles, ligaments, tendons, and Other articles have addressed the various clinical pre­
the various articulations,in particular the sacroiliac joint, is sentations in an effort to come up with a consistent corre­
evident in the literature up to the 1930s and 1940s. Prob­ lation of the various functional disturbances that affect the
ably all of the anatomic structures known have at one time spinal column or the peripheral joints (Brugger 1962,1977;
or another been considered as the source of pain. Mixter Feinstein et aI., 1954; Hohermuth, 1981; Jones, 1981;
and Barr (1934), however, rather than presenting a single Mitchell et al., 1979; Sutter, 1975; Sutter and Frohlich,
case study or a listing of empirical observations, introduced 1981; Waller, 1975; Dejung, 1985; Dvorak et aI., 1987c;
a well thought-out series from the "base of the skull down, Southwick and White, 1983; Herron and Turner, 1985;
covering the 'waterfront.' Cervical, dorsal and lumbar le­ Mattie, 1986). Simons (1976 a, 1988) has presented an ex­
sions were all included in this first article" (Barr, 1977). haustive summary of the many reports in the literature that
Attention and effort thereafter, so it seems, were pri­ relate the muscles and fascia to the various pain syn­
marily directed toward the subject of the herniated inter­ dromes, while at the same time posing the question
vertebral disk and its role in the radicular pain syndromes. "Why should so common and serious a problem be so
This ultimately steered attention away from muscle and neglected by modern medicine?" (Simons, 1988).
other soft tissues and toward nerve root compression as a The ideal is to identify those clinically meaningful pa­
cause of pain (Gerwin, 2000). rameters and diagnostic criteria that would unequivocally
In the most recent two or three decades,however, there assist in distinguishing from true radiculopathies the pain­
has been a noticeable trend in which both the "old" or ful nonradicular musculoskeletal syndromes that mimic or
orthodox branches of medicine and the "new" or alterna­ are similar to the explicit radicular syndromes. This should,
tive health-care counterparts alike have shown particular at least in theory, facilitate the proper choice of therapy for
interest in investigating many of the nonradicular pain a particular disorder, clinical presentation, or syndrome.
syndromes. The exact reasons for this rising interest are For the field of manual medicine this means that one goal
not entirely clear. is to determine which approach or technique(s) are best
Many published reports have attempted to organize and suited for a particular patient, ranging from such varied
categorize the seemingly countless descriptions of the ap­ maneuvers as the high-velocity, low amplitude manipula­
parently diverse painful soft-tissue disorders and nonra­ tions (thrusting techniques) to the "gentle" approaches of
dicular pain syndromes. The terminology seemed to get in soft-tissue techniques, including the various trigger point
the way, as many previous accounts had been categorically and tender point approaches, myofascial release tech­
lumped under such nonspecific terms as inflammatory niques, muscle energy or facilitatory techniques, among
soft-tissue rheumatism. Although seemingly similar so­ many others. There already exist a number of good, rational
matic phenomena appear to have been described by the rehabilitation approaches that ultimately should allow the
various authors over the years, the language and terminol­ patient to undertake the transition to an independent
ogy used often seemed to reflect more the individual au­ home exercise program as soon as the clinical situation
thor's opinion or that of a particular school of thought than allows.
a common scientific language. The sheer number of the At an international manual medicine seminar in Swit­
many neurophysiologic hypothetic al postulates, coupled zerland in 1983, now known simply as the "Fischingen
with the often confusing, nonstandard language, which Conference," an attempt was made to collate, correlate,
also varied from country to country may, at least in part, and unify the different terminologies used by the many
explain why even clinically relevant observations might schools of thought and practice (Dvorak and Dvorak, 1984).
have been lost or hitherto ignored. From a historical per­ In this chapter we want to present five models that deal

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Nonradicular Pain: Spondylogenlc and Myofascial Pain Syndromes

with the various components of the nonradicular spondy­ structures. When injecting hypertonic sodium chloride so­
logenic or musculoskeletal pain syndromes as they relate lution into the paravertebral muscles, the ligaments, and
to the field of manual medicine: the apophyseal joints (also referred to as the facet or zyg­
apophyseal joints), or when scratching the periosteum
1. Referred pain. with a needle, localized and referred pain was consistently
2. Myofascial pain syndromes. elicited that was in accordance with the segmental inner­
3. Postural pseudoradicular syndromes. vation (Kellgren 1938, 1939; Lewis and Kellgren, 1939)
4. Somatic dysfunction and tender points. (Fig. 6.1).
5. Spondylogenic reflex syndromes. When the deep structures were stimulated, a rather
diffuse pain distant from the origin of stimulation was
Despite the diversity in terminology, the attentive reader observed. When certain areas of the thoracic spine were
will readily recognize the overlap of, and the similarities stimulated, pain was referred to both the anterior and
among. the different descriptions of the various clinically posterior portions of the trunk in a patchwork pattern
observed phenomena and the postulates of the proposed that is similar to skin hypersensitivity (Fig. 6.2) (Hockaday
neurophysiologic mechanisms. and Whitty, 1967). This is in distinct contrast to other types
of thoracic pain that may follow a band like or girdle dis­
tribution as seen in some neuropathic pain states, such as
Referred Pain pain associated with herpes zoster.
Stimulation of various structures at the lumbosacral
Referred pain, in the simplest terms, may defined as pain junction produced a deep pain both in the gluteal region
that is perceived by the patient at a location distant from or and in the thigh, albeit, rarely below the knee.
different from the structure that is presumed to be the pain Skilled palpatory assessment of the muscles, ligaments,
generator. This broad definition includes pain referred and fascia can help differentiate those tissue components
from visceral structures and somatic structures either di­ that are affected as a result of the referred pain and those
rectly or via reflex pathways. Here we describe observa­ that remain untouched by it. It appears that local anesthetic
tions on referred pain originating from somatic skeletal agents applied to the secondarily affected tissues (the
(nonvisceral) structures. muscles, ligaments, fascia, etc.) can reduce the referred
Keligren (1938), Sinclair et al. (1948), and Hockaday and pain level at the referral site. However, the injection of a
Whitty (1967) demonstrated in clinical experiments that local anesthetic agent into the secondarily affected tissues
local and referred pain can be elicited upon mechanical or does not alter the original or spontaneous local pain of the
chemical stimulation of the diverse spinal and paraspinal structure that was initially stimulated (e. g., the supraspi-

Point of stimulation Point of stimulation

"T�
o
o
o
o

L1 "'" L10..... Point

I
-r

rv r) :.
,I --+- +
I

V
• _

b c \
Fig.6.1 Pain pattern upon injection of hypertonic sodium chloride solution into (a) the superficial and (b. c) the deep structures (vertebral
arches, infraspinous fossa of the scapula). (After Kellgren, 1939.)

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Referred Pain

Fig.6.2 Diagram of the patchwork


distribution of referred pain after
stimulation of deep structures of the
thoracic spine (vertebral arches,
joints). (After Kellgren, 1939.)

T4

T6

T8 T10
T10
T12
T12
L2 L1

L4 L3
L2

Sl L5
L4

nous or interspinous ligaments). In contrast. when a local tile vertebral segments between (1 and 53, such as the
anesthetic is applied to the area of tile initially stimulated deep muscles and ligaments. The manifestation of referred
ligament, both the local and the referred pain may disap­ pain and the localization of zones with decreased sensitiv­
pear (Kellgren, 1939). Kellgren summarized his experimen­ ity to pain did not always correspond to known radicular
tal observations as follows: innervation patterns such as the zones described by Head,
"The superficial fascia of the back, the spinous processes, and for instance. In Feinstein's studies, the pain was felt mostly
the supraspinous ligaments induce local pain upon stimula­ in the reflexly hypertonic muscles upon injection of the
tion, while stimulation of the superficial portions of the in­ sodium salt solution. This was accompanied by autonomic
terspinous ligaments and the superficial muscles result in a symptoms, such as paleness, excess perspiration, decreased
diffuse type of pain. The deep muscles, ligaments, and peri­ blood pressure, fainting, and nausea, among others.
osteum of the apophyseal joints, as well as the joints them­ Figure 6.3 depicts the various observed patterns of re­
selves, can cause referred pain according to the segmental ferred pain according to the level of segmental stimulation
innervation when sufficiently stimulated." at (4, T4, T6, T11, L2, L4, and L5.
Feinstein et al. (19 54) also injected a hypertonic sodium
solution into tile paravertebral structures associated with

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Nonradicular Pain: Spondylogenlc and Myofascial Pain Syndromes

(4 T4 T4

T6 T6 Tl1

Fig.6.3 Schematic representation of referred pain after injection of hypertonic sodium chloride solution into the deep somatic soft tissues.
(After Feinstein et aI., 1954.)

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Referred Pain

Fig. 5.3 L2 L2 L4 L4
(cant.)

Fig. 5.3
(cant.) L5 L5

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Nonradlcular Pain: Spondylogenic and Myo(ascial Pain Syndromes

1981). This may be of importance for documentation re­


Myofascial Pain Syndromes quirements. for instance, in the patient's medical record, as
not only must the incriminated MTrP be adequately iden­
The myofascial pain syndrome is a muscle pain disorder in tified but also any noticeable functional changes, such as
one or more muscles or groups of muscles accompanied by associated loss of joint range of motion or specific muscle
local and referred pain, and is associated with decreased weakness, or particular objectively verifiable functional
range of motion, weakness, and often autonomic phenom­ deficits (standing, reading, etc.).
ena. Patients are readily recognized by their history of
characteristic muscle pain and the presence of myofascial
Types of Myofascial Trigger Points
trigger points, which are specific areas of hyperirritability
in a muscle that cause local and referred pain on palpation The active MTrP has a low threshold for mechanical stim­
(Meyer. 2002). ulation. With normal physiological motion. local pain ap­
Research during the past 20 to 30 years has provided pears, but it is the referred pain in the reference musculature
valuable information for clinical practice about the painful and fascia that is perceived by the patient as symptomatic.
syndromes associated with the myofascial trigger points The clinically nonsymptomatic latent MTrP refers pain
(Melzack. 1978; Reynolds, 1981; Rubin, 1981; Simons 1975, only when a certain amount of palpatory pressure is ap­
1976b; Travell and Rinzler, 1952; Travell 1976; Travell and plied or when an acupuncture needle is inserted into the
Simons. 1992). MTrP (Melzack, 1981).
The primary MTrP develops independently and not as the
result of trigger point activity elsewhere (Rachlin, 1994).
Myofascial Trigger Points Secondary MTrPs may develop in antagonistic muscles
and neighboring protective muscles as the result of stress
The trigger points may be spontaneously painful or may be and muscle spasms (Rachlin, 1994). We have also observed
elicited upon digital pressure. In the presence of a true secondary MTrPs to develop in synergistic muscles or
myofascial trigger point, the patient describes the per­ muscles of the same functional group, that is, in either
ceived pain in an area that follows a pattern that is the phasic or tonic muscles when one or the other is
characteristic for the particular muscle harboring the myo­ affected. It is common for patients to experience the pain
fascial trigger point (Fig. 6.4). of a secondary trigger point after a primary trigger point is
Similarly to the phenomenon described as the irritation eliminated (Rachlin, 1994).
zone (described below), a specific anatomic or histologic Satellite MTrPs can develop in the area of the referred
substrate has not yet been identified nor have any particular pain as the result of persistent resting motor unit activity in
neurophysiologic interactions that would unequivocally be the muscle (Travell and Simons, 1983a,b). For instance, a
able to explain the development, presence, or perpetuation MTrP in the sternal portion of the sternocleidomastoid
of the individual myofascial trigger point or points. muscle can cause satellite MTrPs in the sternalis muscle,
Hubbard (1993) found spontaneous needle-EMG activ­ pectoralis muscle. and the serratus anterior major muscle.
ity in the myofascial trigger points, which he explained on Little is known about the etiology of the MTrP, but the
the basis of the contraction of the intrafusal muscle fibers. list of the many proposed causes includes direct muscle or
Less convincing were studies that examined local oxygen joint injury. chronic muscle overload, or lengthy periods of
levels, tissue damage, and sympathetic activity in those hypothermia (Travell. 1981). Latent MTrPs can be activated
muscle believed to harbor a trigger point (Bengtsson et by small impulses. such as the overstretching of a muscle, a
al.. 1986, 1989; Bennett, 1989; Boissevian and McCain, sudden burst of muscle activity associated with overload,
1991; Lund et aI., 1986; Simons, 1988; Yunas et aI., 1981). or immobilization. The development of MTrPs in the seg­
mental musculature has been known to occur with com­
pression of the nerve root (Travell, 1976). As a rule, they are
Palpation of Myofascial Trigger Points
not reversible, even after successful operative management
The myofascial trigger point (MTrP) is described as a small (e.g., postlaminectomy syndrome) (Travell, 1976).
area (0.5-1 cm) of muscle that is hypersensitive to pressure There are reports that joint motion restriction (hypomo­
and is noticeably different from the surrounding region bi lity) in the presence of a segmental or somatic dysfunction
when palpated. In normal muscle, a MTrP cannot be dem­ or inflammatory processes can contribute to the formation
onstrated and pain cannot be elicited with normal palpa­ of a MTrP in a muscle or exacerbate it (Reynolds, 1981).
tory pressure. Characteristics of a muscle with a MTrP are
weakness of contraction but no atrophy. Contraction leads Fig.6.4 Examples of trigger points and referred pain in the reference
to decreased motility of the corresponding joint (Travell, sites (pain reference pattern; after Travel! and Simons, 1983 a). I>

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Myofascial Pain Syndromes

Muscles of the Head and Neck Muscles of the Shoulder and Arm

Sterno­ Splenius capitis Infra­ Supraspinatus


cleidomastoid spinatus

Temporalis Masseter

Trapezius Tra pezius Supinator

Extensor
carpi
radialis

Levator scapulae Rectus capitis Interosseus Adductor pollicis


posterior maj or

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Nonradlculor Poin: Spondylogenic and Myofascial Pain Syndromes

Muscles of the Chest and Back Muscles of the lower Extremity

Pectoralis Pectoralis major


major and
minor

· ;i/
+

(,4f \ )
,,fir' .
!li'
:'::.

J
i::
"".,/
)( Trigger point .:;';'. Pain pattern

Fig. 6.4 (cont.)

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Myofascia/ Pain Syndromes

Myofascial Trigger Points and Pain Referral Myofascial Trigger Points:


Patterns Treatment Options

Referred pain, in the presence of either an active or a latent In general, and in addition to standard pharmacologic care
MTrP, is usually very well-localized by the patient. Using (e. g., nonsteroidal anti-inflammatories [NSAIDS], analge­
palpation, the painful muscle or part of the muscle ("myo­ sics), the activity of the MTrP can be addressed specifically
tenone", for definition see below) can be demarcated. The in three ways: (1) introduction of maximal stretch with or
MTrP is described as a "palpable band" (Simons, 1975, without a cooling spray; (2) injection or "dry-needling" of
1976b), which should be palpated perpendicular to the the trigger points; and (3) specific manual medicine tech­
direction of the incriminated muscle fibers (similar to the niques applied to treat the MTrP to the incriminated
"myotendinoses" also defined below). Palpation often muscle or muscles.
causes a local, painful twitch response in the muscle in­ The "spray-and-stretch" method is commonly used to
volved (Simons, 1976a; Travell, 1952). treat the MTrP (Travell, 1981). With the help of a cooling
A MTrP may cause pain in one or in several reference spray (e.g., fluoromethane), afferent nociceptive impulses
sites (Fig. 6.4). of the skin can be invoked, which in turn appear to reflexly
The induction of several so-called satellite MTrPs by a reduce the muscle's resistance to stretch, thereby facilitat­
primary MTrP is described by Travell (1981). For instance, a ing the lengthening of the shortened muscle in the direc­
MTrP in the sternal region of the sternocleidomastoid tion of the normal resting length. This "stretch stimulus"
muscle can cause satellite MTrPs in the sternalis muscle, appears to be able to reduce the activity of the MTrP,
pectoralis muscle, and the serratus anterior major muscle. presumably via the reflex pathways within the spinal
MTrPs can be found in any skeletal muscle; in orthope­ cord, or possibly in higher central nervous system (CNS)
dic practice, a set of common muscles has been regularly centers.
encountered and described (Rachlin, 1994): The MTrP activity can be reduced or even extinguished
by injection of local anesthetics such as procaine or lido­
1. Posterior neck muscles caine. The muscle that harbors the incriminated MTrP
2. Sternocleidomastoid muscle and scalene muscles should be carefully stretched passively during the injec­
3. Trapezius muscle (the most commonly encountered tion. Another form of treatment entirely avoids the need
MTrP in general) for any injectant by approaching the MTrP simply using an
4. Infraspinatus muscle injection needle, a course of treatment known as dry nee­
5. Supraspinatus muscle dling.
6. Levator scapulae muscle, rhomboid muscles, and tho­ Recent reports of the use of botulinum toxin (botox)
racic erector spinae muscles injections have shown some promising results, but further
7. Lumbar paraspinal muscles and quadratus lumborum studies are needed to substantiate the use of this rather
muscle costly procedure. Currently, the use of such injections is
8. Gluteal muscles (minimus, medius, maximus muscles), considered as "off-label" due to diagnostic restrictions.
tensor fasciae latae, piriformis muscle Efforts are under way to determine further specific indica­
9. Rectus femoris muscle and vastus medialis muscle tions and contraindications for the use of botox in muscle
10. Flexor and extensor muscles of the forearm ("golfer's "spasms" and painful myofascial syndromes. Due to the
elbow" and "tennis elbow" syndromes) reported duration of up to 3 months, a possible therapeutic
11. Pectoralis minor and major muscles window is being opened for patients with recalcitrant myo­
12. Interossei foot muscles. fascial pain syndromes, as it would not be reasonable to
inject local anesthetics for prolonged or even open-ended
Other muscles have also been identified as occurring more periods, especially when there is lack of anticipated func­
commonly in the presence of headaches and facial pain. tional progress.
In addition to causing referred pain, the active MTrP can The manual approach to the treatment of various myo­
influence autonomic functions in the reference site, includ­ fascial trigger points is detailed in Chapter 18. A recent
ing cooling by local vasoconstriction or via increased per­ monograph (Dejung et aI., 2003) provides an exhaustive
spiration and amplified pilomotor activity. and well-organized treatise of these methods and the dry­
Occasionally, hyperalgesic skin regions have been ob­ needling techniques.
served (Travell, 1981).

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Nonradicular Pain: Spondylogenic and Myofasaal Pain Syndromes

The Postural Pseudoradicular path of movement. Remember that a reflexly contracted


pectoralis major muscle can easily mimic the substernal or
Syndrome
parasternal pain caused by organic heart disease (Fig. 6.6).
Brugger (1962,1977) coined the term pseudoradicular syn­ Brugger considers the "effort syndrome" as indicative of
drome to differentiate it from the neurologically based the sternal syndrome, representing an abnormal head­
radicular syndrome. The pseudoradicular syndrome is ex­ forward posture.
plained on the basis of the reflex interactions between the In the cervical spine, the reflexly hypertonic neck
various joint structures and the muscles. Of particular in­ muscles may cause a secondary spondylogenic cervical syn­
terest is the potential interaction of some of the somato­ drome. Abnormal sternocostal and sternoclavicular stimu­
motor nociceptors that apparently come into play when lation can also "spread" further to reflexly involve some arm
the soft tissues are irritated or become painful, such as the muscles, which may eventually result in myotendinosis. The
joint capsule or the tendon attachments (Brugger, 1977). reflexogenic changes in the muscles and tendons (myoten­
Brugger believes that the painful reflex nociceptive re­ dinosis) can be demonstrated by having the patient assume
sponses can affect not only the associated muscles and the upright, erect posture position and then the abnormal
their corresponding tendons but the skin as well. The re­ slouched position. The patient may spontaneously report
gion where the muscle-tendon junction has become pain­ that the slouched posture (that is,the patient's stereotypical
ful is referred to as a "myotendinosis." posture) is more comfortable than assuming the normal
Myotendinosis is described as a reflex change in or upright position. This can be explained by the mechanisms
alteration of muscle and tendon function in response to of involving the mechanoreceptor and nociceptor reflexes
pain. These reflex reactions can be initiated by nociceptor as described by Wyke (1979b).
stimulation following: (1) abnormal posture: (2) muscle When the acromioclavicular joints are involved, reflex
and tendon overuse and strain syndromes: (3) direct or myotendinoses have been characteristically noted in the
indirect soft tissue injury: or (4) a combination of these. serratus anterior muscle, the trapezius muscle, the biceps
Brugger (1977) divides the various pseudoradicular syn­ brachii muscle, the coracobrachialis muscle, and the exten­
dromes according to body regions. Upper body involve­ sors of the wrist and fingers (Brugger,1977).
ment includes the sternal syndrome and the thoracic spine It should be noted that the sternal syndrome does not
syndromes. Lower body involvement is comprised of the only affect the musculature of the shoulder, neck, chest,
lumbar syndrome and the symphyseal syndrome. They are and arm but may also present with paresthesias and tro­
described in greater detail below. phic skin changes. Furthermore, and equally important,
Brugger (1977) emphasized that any primary brachial syn­
drome, including the carpal tunnel syndrome and the var­
The Sternal Syndrome ious upper limb overuse syndromes, can all lead to a sec­
ondary sternal syndrome on a reflex basis (Brugger, 1977:
The sternal syndrome is usually the result of a slouched, Gerstenbrand et aI., 1979).
trunk-forward-bent posture that is maintained over a pe­
riod of time. Due to abnormal mechanical loading condi­
tions, the sternocostal and sternoclavicular articulations
are continuously subjected to ever increasing stress and
strain (Fig. 6.5), in particular when abnormal loading forces
are introduced to the thoracic spine and the ribs along with
their connections to the sternum.
As a result of these abnormal loading conditions at the
sternocostal and sternoclavicular joints, the muscles in this
region are increasingly called into action. This can ulti­
mately lead to reflex muscular contraction in many re­
gional muscles including the intercostal, pectoralis major
and minor,sternocleidomastoid, scalene, and the posterior
neck muscles. The involvement of any of these muscles can
relatively easily be assessed by careful palpation.
Starting with the patient in the seated or "normal" up­
a b
right position and requesting him or her to adopt a slouched
posture will provide valuable feedback to the examiner Fig. 6.5 a Slouched trunk position. b Erect (straight) thorax posi-
about which muscles are engaged at what point in the tion. (After Brugger, 1977.)

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The Postural Pseudoradicular Syndrome

Fig.6.6a-d Overview of pain radiation patterns when the sternoclavicular joints (a, b, c, d) and different sternocostal joints (c, d) are
stimulated through puncture (after Brugger, 1962).

and their related myotendinous junctions, particularly in


Reflex Syndromes Associated with the Trunk the pelvis, the abdomen, and the lower limbs. Based on
and the Viscera reports by Fassbender and Wegner (1973) and Fassbender
(1980), Brugger further believes that some of the lumbo­
Functional disturbances of the trunk and disorders of the pelvic dysfunctions can ultimately precipitate new reactive
viscera can both result in myotendinoses and articular inflammatory changes and swelling at the tendinous in­
somatic dysfunction syndromes via somatosomatic and sertions to bone, the tendon sheaths, and the interstitial
viscerosomatic reflex interactions. respectively (Brugger, muscle tissue.
1965). Thus, the confluence of the many somatic sources and
It is known that a primary segmental dysfunction aris­ their secondary reflex interactions at the spinal cord level.
ing from somatic structures can cause pain referral to the at least as seen with the various nociceptive reflex pain
inner organs (Schwarz, 1974), that is, via the somatovisceral patterns, and possibly even at the brain level, may reduce
reflex path. The reverse is also well described, that is. the individual's overall functional capacity, by diminishing
diseases of inner organs can reflexly induce myotendinotic the performance of the entire musculoskeletal system in
changes via the viscerosomatic reflex (Korr, 1975; Beal and general and the other interrelated systems. This, in turn,
Dvorak. 1984). may explain the variability of the many pain syndromes
Proficiency in palpation of the muscles, the fasciae, when they involve the back, the lower limbs. and the pelvis
ligaments and tendons. and, where possible, the nerves, (e. g., shortening of the iliopsoas muscle).
requires solid knowledge of and experience in the func­ Subcutaneous inflammatory processes, hemorrhages,
tional. three-dimensional anatomy. A detailed structural­ and scars can also cause pain that involves the various
functional analysis of body posture and movement patterns articular, muscular, and fascial structures. (Reynolds,
along with appropriate application of local infiltration of 1981). In clinical practice it is often difficult to differentiate
anesthetics in the incriminated spinal joints (apophyseal or between the secondary reflex changes and a presumed
facetjoints) or the costovertebral joints can help distinguish primary musculoskeletal disorder. A detailed and function­
whether the pain arises from a particular musculoskeletal ally oriented structural examination is therefore often a
structure or from a visceral source (Wyke, 1979a, b). logical place to start in order to assess the current states
of the different structures, at the time of presentation in the
office. The assessment should include a detailed evaluation
Syndromes of the lower Body of the incriminated muscles, the tendons. ligaments, fas­
ciae. and joint capsules.
According to Brugger (1965). the functional unit of the Stimulation or irritation of the apophyseal joints in the
lower body consists of the thoracolumbar spine, the pelvis, thoracolumbar and the lumbosacral junctions can cause
and the lower limbs and the corresponding regional back particular myotendinotic pain patterns in the muscles
muscles and the abdominal muscles. and tendons associated with the spine, the abdomen, and
Abnormal mechanical stress to the lumbosacral junc­ the lower limbs (Fig. 6.7).
tion. for instance, may preferentially affect certain muscles

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Nonradlwlar Poln: Spondylogenlc and Myofascial Pain Syndromes

,:. :.. .
::
. :I
r';;,t . :
.
" '
" "I .,'•.
..

. .: '.
00' "I • •

:
• . .

. ...:.
"

. .

. .-
·

' . ....
: " "
· · ·
'

' "

I
,
I
I
I
I
l

Fig.6.7 Pain radiation pattern when different apophyseal joints are stimulated through puncture. (After Brugger, 1962.)

Symphyseal Syndrome femoris muscle, sartorius muscle, tensor fasciae latae


muscle) (Brugger, 1962, 1977) (Fig. 6.8).
In the slouched sternosymphyseal posture as described
by Brugger (Fig. 6.9), the synergism between the paraspinal
extensors and the abdominal wall muscles is displaced in
favor of the abdominal muscles, which in turn may further
exacerbate the already present irritation at the symphysis.
It is often impossible to distinguish on clinical grounds
only a primary symphyseal disturbance from the many
possible painful secondary and adaptive reflex changes
invoked by the various ligaments and the tendon­
periosteum interface at the symphysis, when the cause
may be due to disturbances in the thoracic spine, for in­
stance.

Fig.6.8 Pain radiation when the symphysis pubis is stimulated To recognize a true radicular syndrome and to be able to
through puncture. (After Brugger, 1962.) differentiate it from other sources that can' mimic it, the
clinician should at least be aware of that articular or so­
It has been reported that the infiltration of the symphysis matic dysfunctions, e, g., in symphysis pubis, can lead to
pubis with local anesthetics can lead to the immediate pain due to reflex myotendinotic reactions. Thus, even a
disappearance of symptomatic pain in the pelvis or the "simple" slouched posture may precipitate an adaptive or
legs. This would indicate that both the symphysis and the compensatory "downward spiral" cascade that may cause
pelvis are potential pain generators. Dysfunctions involving pain easily mimicking a true radiculopathy (Fig. 6.10),
the symphysis pubis or the entire pelvis may ultimately When involved in the symphyseal syndrome, the por­
lead to painful myotendinotic reactions in the lumbar para­ tion of the longissimus thoracis muscle that spans between
vertebral muscles ("symphyseal lumbago"), in the muscles the sacrum and the mid-thoracic spine may become painful
of the pelvis and the abdomen (symphyseal abdominal wall and refer pain not only to the spine itself but also to the
pain), or in the muscles of the lower limb (e. g., quadriceps interscapular region due to the reduced tone ("hypotoni­

124

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The Postural Pseudoradicular Syndrome

city") and the subsequent associated myotendinotic reac­


tions. To counteract the backward tilt, the iliopsoas muscle
must be recruited and may then be continuously con­
tracted. The tensor fasciae latae, sartorius, and rectus
femoris muscles act synergistically. The hamstring, calf
muscles, and the fibular (peroneal) muscles may become
painfully hypotonic, or reflexly weak. It is therefore not
surprising that a myotendinotic pain syndrome that devel­
ops in this fashion can easily be mistaken for a lumbar
radiculopathy.
The palpatory and functional examination of the various
muscle groups should be performed with the patient as­
suming a slouched posture and in the upright-erect posture
as well as the supine position. Interestingly, some of the
myotendinotic reactions often seem to disappear when the
patient assumes an upright posture, especially when the
a b
examiner supports such a posture by broad hand place­
ment on the patient's posterior trunk for stability. However,
as mentioned, a number of patients may find the erect Fig.6.9 a A torque acting in the posterior direction when the
posture as less comfortable. patient is in the slouched sternosymphyseal position.
Figure 6.11 provides an overview of some of the possible b Disappearance of the torque in the pelvic region when the patient
is sitting erect. (After Brugger, 1962.)
nonradicular pain radiation patterns encountered with ir­
ritation of various joint capsules.

Fig.6.10 Muscles that are involved in extension of the trunk (red) and muscles involved in the slouched position (blue). (After BrLigger,
1962.)
a SloLiched, sternosymphyseal position.
b Erect position.
_ Muscles responsible for trunk extension.
_ Muscles participating in perpetuating the sternosymphyseal slouched position.

125

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Nonradicular Pain: Spondylogenic and Myofascial Pain Syndromes

Fig.6.11 Pain radiation pat­


tern when different joint cap­
sules are stimulated by way of
puncture. (After Brugger,
1962.)

The goal of the practitioner is to detect abnormal joint


Somatic Dysfunction and Tender Points function with regard to asymmetry in range of motion,
usually that of hypomobility rather than of hypermobility,
In the osteopathic manual medicine literature and practice, and tissue alterations such as "bogginess" (thickness, in-
the central consideration for diagnosis and treatment of the creased consistency), heat, and perspiration, among others.
nonradicular pain syndromes of spondylogenic and myo- Although these findings are typically associated with local-
tendinotic origin is the somatic dysfunction (Korr, 1975; ized tenderness or palpatory pain, pain itself is not the
Mitchell et aI., 1979; Jones, 1981; Greenman, 1996). "sine qua non" in the osteopathic understanding of the
Somatic dysfunction is defined as impaired or altered somatic dysfunction.
physiological function of related components within the The diagnosis of a segmental vertebral dysfunction or
somatic (body framework) system including the skeletal. somatic dysfunction is based on a targeted structural and
arthrodial, and myofascial structures, and the related vas- functional musculoskeletal examination that expands upon
cular, lymphatic, and neural elements. This definition, the standard neuro-orthopedic examination. The structural
which replaces the antiquated term "osteopathic lesion," and functional examination, in essence, represents a thor-
was registered with the International Classification of Dis- ough and at the same time refined assessment of the
eases under the number 739. various components of the axial and peripheral articular

126

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The Spondy/ogenic Reflex Syndrome

system, looking for relevant asymmetries in form and func­ they may be compared to the latent phase of the interver­
tion, which may be amenable to manual medicine treat­ tebral insufficiency, as described by Schmorl and Jung­
ment procedures or specific rehabilitative exercise rou­ hanns (1968).
tines. The goal of the structural-functional examination is The results of the positional examination dictate the
to arrive at a germane segmental diagnosis that is of suffi­ direction of the manual therapeutic approach for the ten­
cient clinical significance within the entire clinical presen­ der points. After careful localization of a particular tender
tation to be treated in one form or another. While many point, the patient's limb, or head, neck, trunk, or pelvis is
practitioners may base their findings on the presence of positioned such that the initially reported tenderness is
localized pain, such as that associated with a tender point significantly reduced in a specific position (at least 70%
(described below), the convention in osteopathic practice is intensity reduction), The examiner may find that in re­
to determine motion restrictions and soft-tissue abnormal­ sponse to proper treatment the initially palpated soft­
ities first and to treat those without "chasing the pain" tissue "tension" is also reduced accordingly, and the tender
(Greenman, personal communication 1983), A second, but points should no longer be painful or be only minimally
equally important, diagnostic goal is to determine the po­ painful to the patient. Again, there are a number of sim­
tential relationships of various findings in different spinal ilarities with the definition of the tender points and the
regions and the limb joints and muscles, and if possible to entity called the "irritation zone."
ascribe the findings to adaptive or compensatory mecha­ The growing understanding of the somatic dysfunction
nisms. complex as such and the particular attention paid to the
One of the neurophysiologic postulates about the occur­ detailed soft-tissue examination using refined palpatory
rence of segmental motion restriction with soft-tissue techniques, for instance, prompted the introduction of a
changes is that of the "facilitated segment." which is number of new treatment concepts in osteopathic medi­
thought to explain some of the chronic changes noted in cine, such as the "muscle energy technique" (MET) (Mit­
the affected spinal section and at the segmental level (Korr, chell et aI., 1979), the "strain and counterstrain" technique
1975), (jones, 1964, 1981), and the myofascial release technique
One of the possible, but not universally required, clinical (Ward and Clippinger, 1987). Similar to, yet different from,
manifestations of a somatic dysfunction is the presence of these techniques are the muscle facilitation and inhibition
what Jones (1964, 1981), and before him Kellgren (1938), techniques introduced by Lewit (1981). While the "cranio­
refers to as the tender point. Such tender points can provide sacral" techniques have been described in early osteopathic
clinically relevant information for the diagnosis of abnor­ literature, and despite their ever-increasing popularity,
mal joint function arising from either the apophyseal or the they remain controversial, even within the circles of man­
peripheraljoints and can guide the palpatory evaluation of ual medicine practitioners (Greenman, 1996).
the associated reflex changes in the incriminated soft tis­
sues.
The tender points described here, and which are to be The Spondylogenic Reflex Syndrome
differentiated from tender points associated with fibro­
myalgia syndrome, are usually painful upon palpatory Numerous empirical reports in the literature give an ac­
pressure, The patient may characterize the pain upon pal­ count of apparent relationships between the axial skeleton
pation as a stabbing type of pain, Typically, and unlike a and the peripheral soft tissues that are difficult to explain
myofascial trigger point, these tender points do not refer solely on the basis of neural or radicular, vascular, or en­
pain spontaneously, They can be palpated as enlarged or docrine mechanisms.
"boggy" tissue changes. The points, while typically located Following his clinical observations, Sutter (1975)
at specific regions that have been found to correspond to presented a concept he termed "the spondylogenic reflex
specific articular levels, are usually in close proximity to the syndrome" (Greek, spondylos = vertebra). The spondylo­
affected joint. They are mostly to be found in the deeper genic reflex syndrome (SRS) is thought to arise from an
muscle layers, and their size does not normally exceed 1 cm articular dysfunction involving either the facet joint (apo­
in diameter. physeal joint) or a peripheral joint when it affects a limb.
With spondylogenic dysfunction, they often appear Due to the associated motion restriction, e. g" hypomobility
multiply, primarily in the paravertebral region, often at or abnormal functional position or dysfunction of the facet
the same level as the related articular processes. They are (apophyseal or zygapophyseal)joint, certain reflex changes
also found on the anterior side of the trunk (Fig. 6.12). can be invoked that may eventually lead to anatomically
Tender points have been described for a number of joint localizable, noninflammatory changes in the soft tissues
dysfunctions. Even with subclinical disturbances, they have associated with the incriminated joint. The articular dys­
been reported to be detectable by careful palpation, Thus function is thus believed to be a disturbance at the "internal

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Nonradicular Pain: Spondylogenic and Myofasdal Pain Syndromes

a b

Fig.6.12 Localization of selected posterior tender points (exam­ Note: There are cu rrently over 200 such points considered as
ples). (After Jones, 1981.) tender points (after Jones).
a Posterior. b Anterior.
1 (1 1 Acromioclavicular joint
2 T2 2 (7
3 T3 3 Sternoclavicular joint
4 Ribs 4 Tl-T6
5 Tl-Tl2
6 L1- L3

functional" level of the vertebral spinal unit of the affected perpetuating the controversy about its very existence.
facet joint. The vertebral spinal unit, also Imown as the Again, the articular or somatic dysfunction should be
spinal motion unit, consists of the two vertebral joint part­ viewed as the expression of a reversible motion restriction
ners and their joints with the intervening intervertebral with possible soft-tissue changes in the incriminated spinal
disk. In the articular dysfunction, there is a disturbance of segment or spinal region, the objective clinical detection of
both the static and the dynamic balance between the in­ which is accomplished through the process of specific
dividual bony parts that make up the axial skeleton such as static tissue and dynamic motion palpation.
the skull, the vertebrae, and the pelvis, and the related The primary afferent sources of the SRS are the inter­
muscle-tendon system. Maigne (1970) refers to these dis­ vertebral or facet joints (apophyseal or zygapophyseal
turbances as "derangements intervertebrales mineurs." joints). When the joint-associated mechanoreceptors and
The osteopathic literature refers to similar entities as the nociceptors in the joint capsule, ligaments, and muscles are
somatic dysfunction complex. stimulated above their normal threshold for a prolonged
As the individual motion restriction may be rather period, the invoked reflex pathways (CNS) will bring about
small, but nonetheless potentially clinically relevant, the valuable soft-tissue changes that can be clinically observed
"faulty vertebral position" associated with a particular ar­ and correlated within the particular clinical presentation
ticular dysfunction cannot usually be identified or detected (Waller, 1975; Wyke, 1979b).
on adjunctive diagnostic studies such as standard radiog­ One of the first demonstrable clinical manifestation of
raphy or MRI. This is in stark contrast to the easily recog­ the spondylogenic reflex syndrome is the so-called irrita­
nizable structural changes seen with even very minimal tion zone (Caviezel, 1976). Other authors have referred to
scoliosis or anterior-posterior spinal deformities. The similar changes as the segmental points (Sell, 1969), para­
difficulty of demonstrating an articular dysfunction on vertebral points (Maigne, 1970), or the previously men­
radiographs, for instance, may partly have contributed to tioned tender points Uones, 1981).

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The Spondy/ogenic Reflex Syndrome

may mean many things to different people, including the


Irritation Zone
description of tightness, hypertonicity, and even normal,
The irritation zone represents small. painful soft-tissue albeit increased, muscle tone. Within the context of this
changes that, when palpated, can be quite tender even text, the description by Rachlin (1994) is adopted to de­
when the applied pressure is minimal. It averages between scribe myospasm: myospasm is a clinical description of
0.5 and 1 cm in size. The irritation zones are located in increased tone affecting an entire muscle that has become
topographically well-defined areas or regions at the level painful due to an involuntary contraction. In addition to the
of the muscular and fascial tissues. The main characteristic pain, the myospasm usually causes the muscle to be short­
is the direct relationship between the temporal and qual­ ened, limiting the associated range of motion. In the Ger­
itative response of the irritation zone and the severity of man literature this phenomenon is described as "myosis"
the associated articular dysfunction. That is, as long as the (Myose), but there is no equivalent term in the English
articular dysfunction is not eliminated or effectively cor­ literature. The muscle that is affected by myospasm is
rected, there will be a clinically identifiable irritation zone. palpated perpendicularly at its belly, whereas it is palpated
However, once the disturbance has been corrected, the longitudinally at its origin and insertion.
irritation zone disappears quite promptly. This is of clinical A generalized increase in muscle tone in the absence of
significance, in particular in the patient management pro­ muscle pain (either spontaneous or upon palpation) is
cess while monitoring patient response. known in the German literature as Hartspann, which trans­
Again we emphasize that when we speak of an irritation lates as "hard tension." Thus, we may use the term muscle
zone we refer to a clinical entity on the palpatory expres­ tension (or increased muscle tone or hypertonicity) simply
sion of joint function through the various soft tissues. To as a description of a change in muscle tone while the
date, no anatomic or histologic substrate has been identi­ muscle is contracted, while not necessarily being painful.
fied that would be pathognomonic for the irritation zone. A relaxed healthy muscle, when palpated, displays a
Among the most important causes of an articular dys­ characteristic firmness, consistency, and plasticity. The in­
function are previous trauma, muscular imbalance and dividual muscle bundles usually cannot be differentiated
uncoordinated or inappropriate movement patterns, acute from each other by palpation except than when separated
and chronic mechanical overload of the vertebrae, and by the various fascial septa. When the muscle is affected
osteoligamentous insufficiency. Secondary articular dys­ and shows signs of prolonged increased tone, it is often
functions in response to inflammatory or degenerative said to be "in spasm." When "in spasm," that is, it is con­
joint disorders, including microfractures, or those associ­ tracted for some period of time, the muscle reveals in­
ated with space-occupying lesions, should routinely be creased "bogginess" (thickness, increased consistency)
considered in the comprehensive management of the var­ often associated with increased resistance to allow stretch,
ious painful syndromes (Northup, 1966). and diminished plasticity. Either the entire muscle or only a
Thus, in the authors' view, the term articular or somatic few muscle bundles in the longitudinal direction can be
dysfunction may represent a more specific and potentially affected. On palpation perpendicularly to the muscle fibers
clinically more relevant diagnosis than the current usage of with average pressure, the myospasm may become painful
"sprains and strains" so commonly "diagnosed" in conjunc­ and can be relatively easily differentiated from the sur­
tion with the various spinal pain syndromes. rounding area of the same muscle portions that are not
Noteworthy sequelae associated with the various artic­ directly affected. A myospasm can be followed with palpa­
ular or somatic dysfunctions arising from reduced facet tion from the origin to the insertion of the involved muscle
mobility are the noninflammatory "tendinoses" and the in a longitudinal manner. "Nervous misinformation" from
"myotendinoses," which, in our understanding, represent the involved muscle bundles (Fassbender, 1980) has been
abnormal soft-tissue changes of the tendons and muscles proposed as the mechanism underlying the reflex path­
respectively. They are identified by specific and carefully ways responsible for the origin of the involuntary isometric
performed palpation. increase in muscle bundle tone (Fig. 6.13).

Myotendinosis and Myotenone


Myospasm and Myotendinosis
When there is continued increased muscle tone in the form
of long-standing myospasm, the involved muscle-tendon
Myospasm
unit can undergo myotendinotic changes. The myotendi­
While commonly used in clinical practice, the term "muscle notic changes affecting the muscle and/or tendinous inser­
spasm" or "myospasm" has not been specifically defined as tions can be caused by uncorrected segmental dysfunc­
to underlying pathophysiologic changes. As used, the term tions. In the field of rheumatology this has often been

129

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Nonradicular Pain: Spondylogenic and Myofascial Pain Syndromes

referred to as noninflammatory soft-tissue rheumatism


Segmental dysfunction (Fig. 6.14).

l
Again, myospasm is a clinical term used to describe a
state of painfully increased tone in muscle that can be
elicited by palpatory pressure or that may appear sponta­
Stimulation of mechanoreceptors
and nociceptors neously. Painful myospasm is principally found in the
muscle belly, while the associated changes can involve

l
Reflexes via eNS
the entire length of muscle or where the muscle fibers
change their direction. They are also found at the free
- "Misinformation"
muscle borders such as the trapezius muscle, and pectoralis

l
Myotendinosis
major muscle, for instance. With continued, nonphysiologic
excitatory impulses and in response to a continuously in­
creased tone, it is plausible to assume that the muscles
compensate as long as possible, to the point of overcom­
Fig.6.13 Development of increased muscle tone (hypertoniCity).
pensation until the inherent adaptive mechanisms fail and
(AFter Fassbender, 1980.)
the muscle actually starts to decompensate (Fassbender
and Wegner, 1973; Fassbender, 1980). The decompensation
then ultimately leads to muscle tears and overt rupture,
====--== =- L potentially resulting also in significant damage to the af­
fected myofascial components associated with the partic­
1 ular muscle (Fig. 6.15).
a Attachment tendinoses represent localized swelling of
tendons at the respective origin and insertion. They can

"";: ' 1 ....-


.. t - be extremely painful upon even minimal palpatory pres­
'l :':.'--=-::::
_ :=:'::-- ' 1 -1' -")l·-'; .::
: :ti",==-- ........- sure. The hallmark is their mirror-image appearance: that

; ;,
-- ___

' :':'::
b
'.
T is, presence at both the muscle's origin and its insertion. In
addition to the characteristic points at the respective at­
tachment, the tendinoses can also be found at the muscle­
Fig.6.14 tendon junction of the incriminated muscle.
a Schematic representation of a normal muscle. Morphologic studies have revealed that due to the pre­
b Muscle that has become painful with increased tone (myo­
sumed relative hypoxia in the involved muscle there is
spasm).
anomalous development of the mesenchymal connective­
tissue cells (Fassbender, 1980; Fassbender and Wegner,
1973) (Fig. 6.15).

L
P ermanently increase Myotendinosis
tonus in the muscle Tendinoses and painful myospasm as a rule do not occur
unexpectedly as they take quite some time to develop
enough to be noted clinically. One mechanism is thought
+ 0, req ui e
J
r m ent but to be the result of various reflex interactions. Correspond­
Overload at the tendons
normal 0, supply ingly, once the causative disturbance has been eliminated,
the tendinoses and myospasm are expected to disappear
after a certain latency period (referred to as "latent zones"
Relative hypoxia
] [ Localized lack of 0, by Sutter). This helps in differential diagnosis to set it apart
from the presence of the irritation zone. Also, clinically,
they must be differentiated from other secondary trau­
Degenerative
fiber damage
I Progressively degenerative
tendon changes
matic myospasms and myotendinoses.
a b Each muscle or muscle part can independently undergo
myotendinotic changes. Such a clinical muscle-unit with
Fig.6.15 Pathogenesis of noninFlammatory soft- tissue rheuma­
the corresponding tendons is referred to as myotenone.
tism. (After Fassbender and Wegner 1973.)
a Myospasm. Slender muscles represent a single myotenone. Broad,
b Tendinosis (tendonopathy). flat, and fan-shaped muscles comprise several myotenones
(Fig. 6.16).
Clinical experience has shown that certain axial skeletal
components are correlated with specific myotenones.

130

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The Spondy/ogenic Reflex Syndrome

L3

Rectus capitis O bliq u us


posterio r capitis
minor superior

Gluteus
medius

(1
___--'-<E: IE'--
-- 0 bliquus
(2 c a pi t is
inferior

TlO

a b

Fig.6.16
a Individual myotenones.
b Myotenones in a fan-shaped muscle.

which can be objectively verified by palpation. A functional


The Postural Spondylogenic Reflex Syndrome:
disturbance in one vertebral unit usually brings about myo­
tendinotic changes in the empirically correlated myo­ Clinical Correlation with Reflexes linked to
tenones. Since the spondylogenic-reflexogenic myotendi­ Nociceptors and Mechanoreceptors
noses can be routinely identified. they are collectively
termed systematic myotendinosis (Sutter and Frohlich. The clinical symptom of pain in muscles and other soft
1981; Travell and Rinzler. 1952). The primary articular or tissues. be it spontaneous pain or pain elicited with palpa­
segmental (somatic) dysfunction of a vertebral segment. tory pressure. has been termed the spondylogenic reflex
when followed by myotendinotic changes. represents the syndrome by Sutter (1974.1975). Likewise the authors have
primary SRS. been able to observe the various systematic myotendinoses
Under certain circumstances additional secondary. ter­ in response to an articular/somatic dysfunction involving
tiary. and other SRSs can develop in a chain-reaction se­ the individual apophyseal. occipito-atlanto-axial. and sa­
quence. Thus. many factors can play a crucial role in the croiliac joints. We have observed that many systematic
development of the spondylogenic reflex system. These myotendinoses improve during the course of therapeutic
include spinal deformities. abnormal or stereotypic motion intervention in the individual patients. It was therefore
patterns. muscle and proprioceptive imbalance. loss of assumed that. in addition to other helpful physical and
muscle strength. and inherent articular dysfunction. In therapeutic procedures. the mechanical and functional cor­
clinical practice. many of these factors may be in play rection of the spinal motion unit according to Schmorl and
together and in simultaneous combination represent a Junghanns (1968) can play a significant role. if not the most
rather complex clinical picture. crucial role in treatment.
Therefore. and almost routinely. it is not possible to Wyke's observations (Wyke. 1979a. b) and research in
determine the causative primary SRS. especially in patients the new field of articular neurology have brought signifi­
with chronic conditions. The primary SRS may actually cant insight into some of the principles underlying the
have "resolved" only to give way to the secondary SRSs. diagnostic and therapeutic approaches in the field of man­
which should then be considered the new primary syn­ ual medicine. In a clinical study of adolescents. we found
dromes (Travell. 1981). The characteristic features of the that the absence of pain does not automatically mean lack
irritation zone are listed and compared with the spondylo­ of soft-tissue findings. It is well known that localized pal­
genic myotendinosis in Table 6.1. Careful examination tech­ pable muscle bands or systematic myotendinoses can be
niques and precise anatomic knowledge are necessary for elicited upon careful palpation in many individuals who
establishing the correct diagnosis and initiating the appro­ have no subjective pain complaints. According to the au­
priate therapy.